Alternative Ways to Treat Crohns Disease

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. 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. Continue reading...

No More Crohns Disease Summary


4.6 stars out of 11 votes

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Author: Cathy Rubert
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My No More Crohns Disease Review

Highly Recommended

The writer presents a well detailed summery of the major headings. As a professional in this field, I must say that the points shared in this book are precise.

As a whole, this book contains everything you need to know about this subject. I would recommend it as a guide for beginners as well as experts and everyone in between.

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

Contents: Ebook
Author: Alec Herring
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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

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Breakthrough Crohns Disease Guide

In Breakthrough Crohn's Disease Guide, you'll learn how your digestive system really works absorbing nutrients and fluids from the foods you eat while compacting and sending waste products along their way. You'll discover how your own immune system, in trying to fight a perceived threat, has sent white blood cells to the smooth lining of your digestive tract where they do their best to root out infection. Continue reading...

Breakthrough Crohns Disease Guide Summary

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Author: Sharon Dobson
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Crohns disease and variants of the NOD gene

Crohn's disease was mapped to chromosome 16 by Hugot and colleagues in 1996 in the first genome-wide linkage analysis in this disease using affected pedigrees a total of 25 Caucasian families with at least two affected siblings were analysed using 270 highly polymorphic microsatellite markers across the genome (Hugot et al. 1996). A stepwise approach involving additional families and denser sets of markers resolved a pericentromeric region of chromosome 16, dubbed 'inflammatory bowel disease locus 1' (IBD1). The number of alleles 'shared identical by descent' among affected siblings were analysed, in other words those alleles inherited by both siblings that are copies of the same parental alleles with no assumption about the mode of inheritance. Other investigators subsequently replicated and to some extent refined the region of linkage for IBD1, clearly showing that the linkage was with Crohn's disease and not ulcerative colitis (Ohmen et al. 1996 Cavanaugh et al. 1998 Cavanaugh...

Autophagy and Crohns disease

Hampe and colleagues carried out a nonsynonymous SNP scan involving 7159 informative SNPs in 735 Crohn's disease cases and 368 controls with replication of the observed association with ATG16L1 in independent German and UK cohorts (Hampe et al. 2007). Resequencing in affected individuals of exonic, splice site, and promoter sequence of ATG16L1, further genotyping, and haplotypic analysis served to confirm the initial observation that a specific nonsynonymous SNP, rs2241880 (c898A G, p.T300A), was responsible for all the observed increased disease risk at this locus. Possession of the risk G allele resulted in a threonine to alanine substitution at amino acid position 300 in the N-terminal region of ATG16L1 protein. The odds ratio of disease among the German cases analysed was 1.45 (1.21-1.74) no association with susceptibility to ulcerative colitis was found. This result was replicated by Rioux and colleagues in their large genome-wide association scan of ileal Crohn's disease for...

Lessons from inflammatory bowel disease

The elucidation of inherited factors determining susceptibility to inflammatory bowel disease, specifically Crohn's disease, has been a major success story in the field of common complex disease genetics. Pioneering research in Crohn's disease demonstrated the successful application of linkage analysis and a positional cloning approach to identify a specific gene and associated variants in a common disease, while more recent genome-wide association studies have been arguably more successful in Crohn's disease than any other multifactorial disease. The wealth of data now accumulated from such genetic studies have provided radical new insights into Crohn's disease pathogenesis and individual susceptibility. Why has Crohn's disease been such a success story The answer is unclear, but compared to many common diseases the evidence for a significant role for inherited factors is strong, the disease phenotype is clearly resolved, and the clinical cohorts studied carefully defined and largely...

A role for inherited factors in inflammatory bowel disease

Crohn's disease and ulcerative colitis are types of inflammatory bowel disease - chronic inflammatory disorders affecting the intestine (Box 9.4). The evidence to support a role for inherited factors is much stronger for Crohn's disease than ulcerative colitis, although clustering of both diseases within families has been recognized since the 1960s (Kirsner and Spencer 1963). A Danish study of 637 patients with inflammatory bowel disease showed that first degree relatives of individuals with either Crohn's disease or ulcerative colitis had a ten-fold increased risk of the same disease (Orholm et al. 1991), while a Swedish study showed that for 1048 patients with Crohn's disease, the risk was even greater with a 21-fold higher prevalence among first degree relatives than the general population (Monsen et al. 1991). Based on many studies, the risk ratio for siblings relative to the population prevalence, Is, is currently estimated at 20-35 for Crohn's disease (Barrett et al. 2008)....

Genetic diversity in ILR pathway genes and inflammatory bowel disease

A number of genome-wide association scans have identified genes in the IL23R signalling pathway as being associated with inflammatory bowel disease, providing important new insights into disease pathogenesis and a potential new therapeutic target. IL23R encodes a subunit of the receptor for IL23. Variants of IL23R at chromosome 1p31 were identified from a genome-wide association study of individuals with Crohn's disease of European ancestry in North America (Duerr et al. 2006 Rioux et al. 2007) and subsequently

Genomewide association studies and inflammatory bowel disease

Perhaps of any common multifactorial disease, the greatest success seen to date with genome-wide association studies has been with Crohn's disease. From 2005 to 2008, the number of clearly replicated and defined genomic loci involved in susceptibility to this disease has increased from a widely quoted figure of two (NOD2 at 16q12 and IBD5 at 5q31, although it could be argued this is a conservative interpretation of the linkage data) to more than 30 (Barrett et al. 2008). By 2008, at least seven genome-wide scans have been performed using different population groups and SNP marker sets with extensive replication in independent cohorts (see Fig. 9.22) (Mathew 2008). The concordance between the studies for the most strongly associated loci was striking, as was the relatively modest magnitude of effect size observed. This meant that studies were relatively underpowered to define odds ratios of 1.5 or less (1.3 or below in the case of the largest study, published by the WTCCC). Meta...

Insights from the Wellcome Trust Case Control Consortium study

The WTCCC genome-wide association study of Crohn's disease analysed 469 000 SNPs in 2000 cases of Crohn's disease and 3000 shared controls (WTCCC 2007) (Section 9.3.2). A total of nine genomic loci were associated with disease susceptibility at a genome-wide level of significance, including five previously identified regions NOD2, IL23R, ATG16L1, 10q21 (14 kb telomeric to ZNF365) (Rioux et al. 2007), and a cluster of SNPs in a gene desert on 5p13.1 (Libioulle et al. 2007 WTCCC 2007) (see Fig. 9.22). Apart from IRGM, three other novel loci were found at genome-wide significance. These include SNPs at 3p21 in a region containing many genes, notably MST1 (encoding macrophage stimulating 1 protein involved in inducing phagocytosis), SNPs within NKX2-3 at 10q24.2 (encoding a homeodomain containing transcription factor protein called 'NK2 transcription factor-related locus 3' thought to influence lymphocyte migration and intestinal inflammation), and SNPs upstream of PTPN2 at 18p11...

Inflammatory Diseases

Alicaforsen is example of an AS-ON used as an anti-inflammatory agent, and it is directed against intracellular adhesion molecule (ICAM)-1. ICAM-1 is a cell surface protein that plays an important role in the recruitment of leukocytes to sites of inflammation, and its expression is upregulated in the intestinal mucosa of inflammatory bowel disease (Crohn's disease). Administration of alicaforsen (ISIS 2302) against ICAM-1 results in inhibition of ICAM-1 receptor expression and reduces inflammation (Bennett et al. 1994 Nestle et al. 1994). A few clinical trials using alicaforsen have been reported. In a study reported by Yacyshyn et al. (1998), patients were randomized to receive placebo or alicaforsen. The drug was well tolerated and at the end of the study, 47 of patients in the antisense group went into remission compared to 20 in the placebo group. More recent trials evaluated alicaforsen in patients with active steroid-dependent Crohn's disease (Yacyshyn et al. 2002). A total of...

Insights into the design analysis and interpretation of genomewide association studies

The design and analysis of genome-wide association studies is a complex subject but common themes are emerging as detailed in a number of reviews (Chanock et al. 2007 Kruglyak 2008 Manolio et al. 2008 McCarthy et al. 2008). A number of principles are outlined here, while in the following sections age-related macular degeneration (Section 9.4) and Crohn's disease (Section 9.5) Much work remains to be done through increasingly large genome-wide association scans (of the order of thousands of cases) to define the remaining common variants associated with disease with modest odds ratios (of the order of 1.2). To detect such variants, appropriately conducted meta analysis of comparable scans has proved a powerful approach in diabetes (Zeggini et al. 2008) and Crohn's disease (Barrett et al. 2008). To facilitate this, and to generally promote data sharing, there is a strong consensus that the results of genome-wide association scans should be formally deposited in a transparent fashion. A...

Medical applications and pharmacogenomics

A major goal of current genetic research in the medical arena is to understand how medical care can be tailored to the patient based on their individual genetic makeup. The development of 'personalized medicine' promises significant potential benefits but remains some way from being fully realized. This may be most readily achieved in terms of specific therapeutics, aiming to maximize the benefit for the patient while minimizing the risk of adverse effects. Other applications relate to targeted use of screening and monitoring, for example if an individual is at high risk of colonic or breast cancer, or of hypercholesterolemia, as a result of possession of a particular underlying genetic variant. There are also less direct but potentially equally important applications of current research in terms of our knowledge of underlying disease pathogenesis and potential novel targets for therapeutic interventions. Recent genome-wide association studies in Crohn's disease for example have...

HLAB and susceptibility to ankylosing spondylitis

At 2q13 there was evidence of association with the IL-1 complex (Timms et al. 2004). A study involving 14,000 non-synonymous SNPs more recently showed significant association with IL23R at 1p31 and ERAP1 (encoding endoplasmic reticulum ami-nopeptidase 1) at 5q15 (Burton et al. 2007) the IL23R association is of particular interest given disease associations with psoriasis and Crohn's disease for this locus (Section 9.5.5).

Gene deserts and other loci

The finding of disease associations with SNP markers in regions without any genes (so-called 'gene deserts') is seen for several loci in Crohn's disease as well as other diseases studied by genome-wide association scans. The loci appear highly significant and reproducible in replication studies. For example, Libioulle and colleagues in a genome-wide association scan used 302 000 SNPs to analyse 547 cases and 928 controls in a Belgian population (Libioulle et al. 2007). They found three loci to show strong evidence of disease association with P values between 10-6 and 10-9 IL23R and NOD2, together with multiple SNPs in a 250 kb region at 5p13.1, including four at P

Linkage studies and other inflammatory bowel disease susceptibility loci


Linkage studies in Crohn's disease proved highly informative and have led to the identification of a number of 2007 Barrett et al. 2008). Highly significant association was instead found for rs17221417, a SNP in modest linkage with the 3020insC polymorphism rs2066847, with a P value of 9.4 X 10-12 and an odds ratio of 1.29 (1.13-1.46) for heterozygotes and 1.92 (1.58-2.34) for homozygotes for the risk allele (WTCCC 2007). When rs2066847 was specifically investigated in replication studies it was, however, very significant (P 1.5 X 10-24) and showed the largest odds ratio in case-control analysis of any replicated Crohn's disease risk locus (Barrett et al. 2008). For IBD5 at chromosome 5q31, linkage with Crohn's disease has been reproducibly and convincingly demonstrated and a specific risk haplotype resolved (Rioux et al. 2000, 2001). However, despite intensive efforts at


Figure 9.26 Genetic associations with the IL23R pathway in Crohn's disease. Disease associations have been found for SNPs in genes encoding different proteins involved in this signalling pathway (indicated by asterixes) including the p40 subunit of IL23 the IL23R subunit of the IL23 receptor Janus kinase 2 (JAK2), which is activated on receptor-ligand binding and signal transducer and activator of transcription (STAT3), which is recruited, phosphorylated, homodimerized, and translocated into the nucleus to activate transcription. Reprinted by permission from Macmillan Publishers Ltd Nature Reviews Immunology (Cho 2008), copyright 2008. Figure 9.26 Genetic associations with the IL23R pathway in Crohn's disease. Disease associations have been found for SNPs in genes encoding different proteins involved in this signalling pathway (indicated by asterixes) including the p40 subunit of IL23 the IL23R subunit of the IL23 receptor Janus kinase 2 (JAK2), which is activated on receptor-ligand...


Figure 9.23 Effect of sample size on power to detect common alleles associated with different odds ratios. Three different genome-wide association studies of Crohn disease (Libioulle et al. 2007 Rioux et al. 2007 WTCCC 2007) and a meta analysis (Barrett et al. 2008) were analysed for power to define odds ratios of 1.2,1.3, and 1.5. Power was defined as probability of P A, p.R318Q) that results in an arginine to glu-tamine substitution at amino acid 381. Possession of the glutamine encoding variant was associated with protection from Crohn's disease, with an odds ratio of 0.26 (0.150.43) among individuals of non-Jewish European ancestry (Duerr et al. 2006). The reported associations with Crohn's disease were confirmed by several independent groups (note a number of these relate to rs11465804, an intronic SNP in linkage with rs11209026) (see Fig. 9.22). The same nonsynonymous IL23R SNP, rs11209026, was also demonstrated to be strongly associated with ulcerative colitis (OR 0.53, P 8.9 X...

Genetics of disease

The power of genome-wide association studies in dissecting the genetic contribution to multifactorial traits has been emphasized by studies such as those delineating common variants underlying age-related macular degeneration (Section 9.4) and the Wellcome Trust Case Control Consortium analysis of seven common diseases (Section 9.3.2). There has been an explosion of studies published over the period 2007-2009 utilizing the genome-wide association study approach with considerable success, notably in Crohn's disease and diabetes but also in other traits such as obesity and drug response (Section 9.3). Such studies have been made possible by the carefully phenotyped and curated sample collections that have been established, and by the progress which has been achieved in understanding the genomic architecture of allelic variation, the establishment of panels of informative SNP markers, and the high throughput technologies needed to genotype them. Advances in statistical analysis have been...

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