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The Real Cause of Inflammation/Ulcers In Crohn’s Guts? (SHOCKING)
This is the first of five articles about a completely new way to look at Crohn’s disease.
As I mentioned in my introductory post, the whole idea that Crohn’s is an autoimmune disease is being questioned and even undermined by recent research. For example, the paper below states that CD should be called a chronic inflammatory disorder and instead of an autoimmune disease.
Also, more and more evidence proves Crohn’s sufferers have a WEAK immune response instead of aggressive one that would explain the cause of inflammation and ulcers
Given the above research (and there’s more), we have to seriously question the theory that CD is an autoimmune disease and whether an aggressive immune response is really the cause of the inflammation and ulcers in the guts of CD sufferers. If we are objective, there really is NO evidence to support the current theory of Crohn’s. In fact, all the available evidence suggests the exact opposite: Crohn’s is not an autoimmune disease and Crohn’s sufferers have a weak immune response and not an aggressive one.
So, if an aggressive immune response is not causing the inflammation and ulcers, what is?
Before I share with you what I’m certain is causing the inflammation/ulcers, I want you to consider this fact. There are bacteria that ferment sugars to produce acid that can destroy the hardest substance in our body! In our mouth, bacteria (Strep and others) ferment sugars to produce lactic acid that creates holes in teeth or completely destroys them. A colony of Strep, invisible to the naked eye, can create big hole in a tooth exponentially greater than the size of the colony. So, if bacteria can damage teeth via acid production in such a devastating way, under the right conditions, could bacteria in the guts of Crohn’s sufferers cause the inflammation/ulcers? (It's estimated that there are more bacteria in the gut than cells in the body - that's a lot of bacteria!)
This study shows a link between Crohn's and dental disease.
Here’s what I’m certain is causing the inflammation/ulcers in the guts of CD sufferers. This explanation gets a little technical but it’s well worth the effort to understand it.
Normally, immune cells (macrophages) protect the gut lining from damage by bacteria. However, when there’s too much of protein called TNF (tumor necrosis factor-alpha) in the local environment, it affects their normal behavior and the immune cells don’t protect the gut-lining from damage by bacteria.
Certain bacteria ferment carbohydrates (sugars/starches) and produce acid as a by-product. In Crohn’s, the inflammation/ulcers are CAUSED by acid-producing bacteria along the gut lining. The acid produced by the bacteria BURNS the gut-lining causing the inflammation and ulcers. It’s SHOCKING, I know, but there's overwhelming evidence to support it! Let me show you the evidence by asking a series of questions and then answering them.
If bacteria ferment carbs to produce acid, is there any evidence that sugar/starch consumption is linked to Crohn’s?
ABSOLUTELY! There’s around 12 independent studies from a number of countries that suggest carbohydrates are somehow linked to the onset and development of CD. Here’s just a few.
Is there any evidence that reducing carb consumption improves Crohn’s?
Yes, a recent study, using a diet based on SCD, improved ALL CD patients and virtually all were off anti-TNF medication.
This study used a sugar-free diet for maintenance of remission.
There's also successful studies based on elemental diets. And there's a very significant amount of anecdotal evidence too.
This is a Youtube video of Alex Herring who used a low-carb diet to achieve and maintain long-term remission (8 years plus): http://www.youtube.com/watch?v=o3alTJXEULk
Is there any evidence that bacteria are penetrating the gut-lining and immune cells (macrophages) not removing bacteria from the gut lining?
These papers/studies discuss bacteria penetrating the gut-lining.
Is there any evidence that acid burn is causing the inflammation/ulcers in the guts of Crohn’s sufferers?
Diseased sections of Crohn's guts are typically deformed, thickened and/or scared.
This study discusses stricture formation in Crohn's.
This study discusses stricture formation following acid burn.
This paper discusses gut thickening in Crohn's and which is similar to a rat model where acid was used to induce disease.
Here's some other similarities between Crohn's and acid burn:
Crohn's is linked to vitamin D deficiency low bone mineral density.
Acid burns are linked to calcium wasting and vitamin D deficiency.
Type V collagen is increased in Crohn’s.
Type V collagen in increased in burn tissues.
Proteolytic activity is increased in Crohn's.
Proteolytic activity is increased in burns.
The inflammatory response in Crohn's has been studied for several decades. The inflammatory response in burns has been extensively studied too. Both involve iNOS, PGE2, IL-6, IFN-y expression and much more. I spent a considerable amount of time comparing them and they are the SAME! Here's some specific examples.
IL-22/3 & IL-17 pro-inflammatory cytokines are “fundamentally connected” to Crohn’s.
IL-17 and IL-22 are also found following a deliberate burn.
Th1/Th17 cells are considered characteristic of Crohn's
Th1/Th17 cells can be generated following a burn injury.
Thus, burn injury primed native T cells for an enhanced Th1-type response.
Source: http://www.ncbi.nlm.nih.gov/pubmed/9706148
This year I intend to have analyzed resections from multiple Crohn's sufferers by experts in the field of burns. I'm sure they will conclude that the thickening, deformation and scaring is caused by acid burn.
So, If Crohn’s sufferers eat a low-carb diet will the inflammation/ulcers heal quickly?
Unfortunately, probably not! Normal gut bacteria cause the inflammation/ulcers but something else prevents them from healing or delays the healing process. I will cover this in my next article.
Here's a simple diagram that sums up this article.
This is a potentially a huge breakthrough in Crohn's so let's debate it in an intelligent manner :thumright:
This is the first of five articles about a completely new way to look at Crohn’s disease.
As I mentioned in my introductory post, the whole idea that Crohn’s is an autoimmune disease is being questioned and even undermined by recent research. For example, the paper below states that CD should be called a chronic inflammatory disorder and instead of an autoimmune disease.
“When a disorder like Crohn's disease responds to anti-inflammatory treatment but does not meet accepted criteria of autoimmunity, we submit that it should preferably be called a chronic inflammatory disorder of unknown cause, in which case nothing is implied and nothing is assumed. Emerging genetic and immunological data suggest that Crohn's disease is not an autoimmune disorder...”
Source: http://www.thelancet.com/journals/la...282-6/fulltext
Source: http://www.thelancet.com/journals/la...282-6/fulltext
Also, more and more evidence proves Crohn’s sufferers have a WEAK immune response instead of aggressive one that would explain the cause of inflammation and ulcers
In Crohn’s disease, a constitutionally weak immune response predisposes to accumulation of intestinal contents that breach the mucosal barrier of the bowel wall.
Source: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(06)68265-2/abstract
Source: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(06)68265-2/abstract
The cause of Crohn’s disease (CD) remains poorly understood. Counterintuitively, these patients possess an impaired acute inflammatory response, which could result in delayed clearance of bacteria penetrating the lining.
Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737162/
Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737162/
recent molecular biological and clinical investigations indicate that CD is actually a primary immunodeficiency. 9
Source: http://www.ncbi.nlm.nih.gov/pubmed/20594132
Source: http://www.ncbi.nlm.nih.gov/pubmed/20594132
Given the above research (and there’s more), we have to seriously question the theory that CD is an autoimmune disease and whether an aggressive immune response is really the cause of the inflammation and ulcers in the guts of CD sufferers. If we are objective, there really is NO evidence to support the current theory of Crohn’s. In fact, all the available evidence suggests the exact opposite: Crohn’s is not an autoimmune disease and Crohn’s sufferers have a weak immune response and not an aggressive one.
So, if an aggressive immune response is not causing the inflammation and ulcers, what is?
Before I share with you what I’m certain is causing the inflammation/ulcers, I want you to consider this fact. There are bacteria that ferment sugars to produce acid that can destroy the hardest substance in our body! In our mouth, bacteria (Strep and others) ferment sugars to produce lactic acid that creates holes in teeth or completely destroys them. A colony of Strep, invisible to the naked eye, can create big hole in a tooth exponentially greater than the size of the colony. So, if bacteria can damage teeth via acid production in such a devastating way, under the right conditions, could bacteria in the guts of Crohn’s sufferers cause the inflammation/ulcers? (It's estimated that there are more bacteria in the gut than cells in the body - that's a lot of bacteria!)
This study shows a link between Crohn's and dental disease.
Dental status in CD patients is poor... patients with CD belong to a high-risk group, and preventive measures should be taken early in the course of the disease.
Source: http://www.ncbi.nlm.nih.gov/pubmed/14571099
Source: http://www.ncbi.nlm.nih.gov/pubmed/14571099
Here’s what I’m certain is causing the inflammation/ulcers in the guts of CD sufferers. This explanation gets a little technical but it’s well worth the effort to understand it.
Normally, immune cells (macrophages) protect the gut lining from damage by bacteria. However, when there’s too much of protein called TNF (tumor necrosis factor-alpha) in the local environment, it affects their normal behavior and the immune cells don’t protect the gut-lining from damage by bacteria.
Certain bacteria ferment carbohydrates (sugars/starches) and produce acid as a by-product. In Crohn’s, the inflammation/ulcers are CAUSED by acid-producing bacteria along the gut lining. The acid produced by the bacteria BURNS the gut-lining causing the inflammation and ulcers. It’s SHOCKING, I know, but there's overwhelming evidence to support it! Let me show you the evidence by asking a series of questions and then answering them.
If bacteria ferment carbs to produce acid, is there any evidence that sugar/starch consumption is linked to Crohn’s?
ABSOLUTELY! There’s around 12 independent studies from a number of countries that suggest carbohydrates are somehow linked to the onset and development of CD. Here’s just a few.
A diet high in refined sugar and low in raw fruit and vegetables precedes and may favour the development of Crohn's disease.
Source: http://www.ncbi.nlm.nih.gov/pubmed/519184
Sugar consumption was significantly increased in Crohn's disease
Source: http://www.ncbi.nlm.nih.gov/pubmed/6832625
A high sucrose consumption was associated with an increased risk for IBD
Source: http://www.ncbi.nlm.nih.gov/pubmed/9245929
Our data confirm that patients with Crohn's disease and ulcerative colitis have a high intake of total carbohydrate, starch and refined sugar
Source: http://www.ncbi.nlm.nih.gov/pubmed/7866810
consumption of sugars and sweeteners, sweets...were positively associated with CD risk
Source: http://www.ncbi.nlm.nih.gov/pubmed/15677909
Source: http://www.ncbi.nlm.nih.gov/pubmed/519184
Sugar consumption was significantly increased in Crohn's disease
Source: http://www.ncbi.nlm.nih.gov/pubmed/6832625
A high sucrose consumption was associated with an increased risk for IBD
Source: http://www.ncbi.nlm.nih.gov/pubmed/9245929
Our data confirm that patients with Crohn's disease and ulcerative colitis have a high intake of total carbohydrate, starch and refined sugar
Source: http://www.ncbi.nlm.nih.gov/pubmed/7866810
consumption of sugars and sweeteners, sweets...were positively associated with CD risk
Source: http://www.ncbi.nlm.nih.gov/pubmed/15677909
Is there any evidence that reducing carb consumption improves Crohn’s?
Yes, a recent study, using a diet based on SCD, improved ALL CD patients and virtually all were off anti-TNF medication.
9 out of 11 patients were able to be managed without anti-TNF therapy, and 100% of the patients had their symptoms reduced.
Source: http://works.bepress.com/barbara_olendzki/46/
Source: http://works.bepress.com/barbara_olendzki/46/
This study used a sugar-free diet for maintenance of remission.
Sugar-free diet as long-term or interval treatment in the remission phase of Crohn disease--a prospective stud
Source: http://www.ncbi.nlm.nih.gov/pubmed/6135129
Source: http://www.ncbi.nlm.nih.gov/pubmed/6135129
There's also successful studies based on elemental diets. And there's a very significant amount of anecdotal evidence too.
Although the current medical consensus is that diet is not related to CD, three modern practitioners have independently discovered this perception to be false.
• Robert C. Atkins, M.D. states in his book, Dr. Atkins’ Vita-Nutrient Solution, that he has a 85 percent success rate of treating CD patients with a sugar-restricted (low carbohydrate) diet and high doses of B-vitamins, including folic acid and pantethine.
• Wolfgang Lutz, M.D., a medical clinician in Austria has a success rate of over 90 percent when treating his patients with a low carbohydrate diet for at least one year.
• Elaine Gottschall, M.S. has had remarkable success at healing others suffering from Crohn’s disease and Ulcerative Colitis with a specific carbohydrate diet (SCD), even curing her own daughter.
• John Yudkin, M.D. states in his book, Sweet and Dangerous, that he has successfully used a low carbohydrate diet to treat a variety of gastrointestinal ailments. In one study he achieved a 70 percent success rate.
Source: http://pecanbread.com/healingcrow/dietsmain/crohn/crohn.html
• Robert C. Atkins, M.D. states in his book, Dr. Atkins’ Vita-Nutrient Solution, that he has a 85 percent success rate of treating CD patients with a sugar-restricted (low carbohydrate) diet and high doses of B-vitamins, including folic acid and pantethine.
• Wolfgang Lutz, M.D., a medical clinician in Austria has a success rate of over 90 percent when treating his patients with a low carbohydrate diet for at least one year.
• Elaine Gottschall, M.S. has had remarkable success at healing others suffering from Crohn’s disease and Ulcerative Colitis with a specific carbohydrate diet (SCD), even curing her own daughter.
• John Yudkin, M.D. states in his book, Sweet and Dangerous, that he has successfully used a low carbohydrate diet to treat a variety of gastrointestinal ailments. In one study he achieved a 70 percent success rate.
Source: http://pecanbread.com/healingcrow/dietsmain/crohn/crohn.html
This is a Youtube video of Alex Herring who used a low-carb diet to achieve and maintain long-term remission (8 years plus): http://www.youtube.com/watch?v=o3alTJXEULk
Is there any evidence that bacteria are penetrating the gut-lining and immune cells (macrophages) not removing bacteria from the gut lining?
These papers/studies discuss bacteria penetrating the gut-lining.
In Crohn’s disease, a constitutionally weak immune response predisposes to accumulation of intestinal contents that breach the mucosal barrier of the bowel wall.
Source: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(06)68265-2/abstract
The cause of Crohn’s disease (CD) remains poorly understood. Counterintuitively, these patients possess an impaired acute inflammatory response, which could result in delayed clearance of bacteria penetrating the lining.
Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737162/
Crohn's disease: Bacterial clearance in Crohn's disease pathogenesis
Source: http://www.nature.com/nrgastro/journal/v7/n3/full/nrgastro.2010.1.html
This study found that immune cells were less able to remove dead cells in a TNF-rich environment. If they are not removing dead cells, it's quite possible they are not removing bacteria along the gut lining.Source: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(06)68265-2/abstract
The cause of Crohn’s disease (CD) remains poorly understood. Counterintuitively, these patients possess an impaired acute inflammatory response, which could result in delayed clearance of bacteria penetrating the lining.
Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737162/
Crohn's disease: Bacterial clearance in Crohn's disease pathogenesis
Source: http://www.nature.com/nrgastro/journal/v7/n3/full/nrgastro.2010.1.html
Overall, the data suggest that macrophages in a TNF-alpha- and oxidant-rich inflammatory environment are less able to remove apoptotic cells and, thereby, may contribute to the local intensity of the inflammatory response.
Source: http://www.ncbi.nlm.nih.gov/pubmed/17548650
Source: http://www.ncbi.nlm.nih.gov/pubmed/17548650
Is there any evidence that acid burn is causing the inflammation/ulcers in the guts of Crohn’s sufferers?
Diseased sections of Crohn's guts are typically deformed, thickened and/or scared.
This study discusses stricture formation in Crohn's.
Intestinal fibroblasts in CD possess enhanced capacity for collagen reorganization and contractile activity in vitro. This activity may be responsible for stricture formation in CD.
Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1420964/
Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1420964/
This study discusses stricture formation following acid burn.
Acid burns of the upper gastrointestinal tract produce a complex combination of lesions
Source: http://www.ncbi.nlm.nih.gov/pubmed/8971503
Source: http://www.ncbi.nlm.nih.gov/pubmed/8971503
This paper discusses gut thickening in Crohn's and which is similar to a rat model where acid was used to induce disease.
In areas of gross stricture in CD, the muscularis mucosae comprised almost 10% of total wall thickness. Similar findings were also present in a previously characterized experimental model of CD (trinitrobenzene sulfonic acid-induced colitis in rats), particularly in what appeared to be grossly strictured areas.
Source: http://www.ncbi.nlm.nih.gov/pubmed/2020666
Source: http://www.ncbi.nlm.nih.gov/pubmed/2020666
Here's some other similarities between Crohn's and acid burn:
Crohn's is linked to vitamin D deficiency low bone mineral density.
"Our data suggests, for the first time, that Vitamin D deficiency can contribute to Crohn's disease,"
Source: http://www.sciencedaily.com/releases/2010/01/100127104904.htm
Low bone mineral density is frequently associated with Crohn's disease. Supplementation with daily calcium and vitamin D is associated with increases in bone mineral density. The addition of oral etidronate does not further enhance bone mineral density.
Source: http://www.ncbi.nlm.nih.gov/pubmed/15704046
Source: http://www.sciencedaily.com/releases/2010/01/100127104904.htm
Low bone mineral density is frequently associated with Crohn's disease. Supplementation with daily calcium and vitamin D is associated with increases in bone mineral density. The addition of oral etidronate does not further enhance bone mineral density.
Source: http://www.ncbi.nlm.nih.gov/pubmed/15704046
Acid burns are linked to calcium wasting and vitamin D deficiency.
Thus, burn injury gives rise to calcium wasting, failure of bone to take up excessive calcium, and vitamin D insufficiency to frank deficiency.
Source: http://www.ncbi.nlm.nih.gov/pubmed/22332088
Source: http://www.ncbi.nlm.nih.gov/pubmed/22332088
Type V collagen is increased in Crohn’s.
In strictured intestine both collagen content and the relative amount of type V collagen were significantly increased compared with control intestine.
Source: http://www.ncbi.nlm.nih.gov/pubmed/3335305
Source: http://www.ncbi.nlm.nih.gov/pubmed/3335305
Type V collagen in increased in burn tissues.
Our data demonstrate that type V collagen in preparations from human post-burn granulation tissues consists of 3 alpha chains and can be resolved into 2 distinct heterotrimers.
Source: http://www.nature.com/jid/journal/v87/n4/abs/5614183a.html
Source: http://www.nature.com/jid/journal/v87/n4/abs/5614183a.html
Proteolytic activity is increased in Crohn's.
Proteolytic and leucine aminopeptidase activity levels in faeces from patients with Crohn’s disease and healthy subjects were compared and were found to be 2.5 and 6 times higher, respectively, in patients with Crohn’s disease.
Source: http://www.ncbi.nlm.nih.gov/pubmed/3069527
Source: http://www.ncbi.nlm.nih.gov/pubmed/3069527
Proteolytic activity is increased in burns.
This increased proteolysis may play a role in wound repair and scar formation.
Source: http://www.ncbi.nlm.nih.gov/pubmed/16984440
Source: http://www.ncbi.nlm.nih.gov/pubmed/16984440
The inflammatory response in Crohn's has been studied for several decades. The inflammatory response in burns has been extensively studied too. Both involve iNOS, PGE2, IL-6, IFN-y expression and much more. I spent a considerable amount of time comparing them and they are the SAME! Here's some specific examples.
IL-22/3 & IL-17 pro-inflammatory cytokines are “fundamentally connected” to Crohn’s.
Our findings suggest that activation of the IL-23/IL-17 axis is fundamentally connected to the etiology of CD and may represent the basis for the relapsing nature of the disease by increasing the sensitivity of epithelium to microbial LPS.
Source: http://www.ncbi.nlm.nih.gov/pubmed/18512248
Source: http://www.ncbi.nlm.nih.gov/pubmed/18512248
The Th17 cytokine IL-22 is expressed at high levels in CD and correlates with disease activity
Source: http://www.ncbi.nlm.nih.gov/pubme/18022867
Source: http://www.ncbi.nlm.nih.gov/pubme/18022867
IL-17 and IL-22 are also found following a deliberate burn.
Recently, a novel class of T-helper cells, termed Th-17 cells, has been found to secrete the pro-inflammatory cytokines IL-17 and IL-22.
Source: http://www.ncbi.nlm.nih.gov/pubmed/21353393
Source: http://www.ncbi.nlm.nih.gov/pubmed/21353393
Th1/Th17 cells are considered characteristic of Crohn's
Th1 and Th17 pathways are implicated in Crohn's disease (CD).
Source: http://gut.bmj.com/content/60/Suppl_1/A212.1.abstract
Source: http://gut.bmj.com/content/60/Suppl_1/A212.1.abstract
Th1/Th17 cells can be generated following a burn injury.
Th17 cells critical mediators of host responses to burn injury and sepsis.
Source: http://www.ncbi.nlm.nih.gov/pubmed/22753950
Source: http://www.ncbi.nlm.nih.gov/pubmed/22753950
Thus, burn injury primed native T cells for an enhanced Th1-type response.
Source: http://www.ncbi.nlm.nih.gov/pubmed/9706148
This year I intend to have analyzed resections from multiple Crohn's sufferers by experts in the field of burns. I'm sure they will conclude that the thickening, deformation and scaring is caused by acid burn.
So, If Crohn’s sufferers eat a low-carb diet will the inflammation/ulcers heal quickly?
Unfortunately, probably not! Normal gut bacteria cause the inflammation/ulcers but something else prevents them from healing or delays the healing process. I will cover this in my next article.
Here's a simple diagram that sums up this article.
This is a potentially a huge breakthrough in Crohn's so let's debate it in an intelligent manner :thumright:
Last edited: