23 January, 2006
Neurological disorders: Are they infections?
In one study, 90 percent of the brains of Alzheimer's victims contained the pneumonia bacteria, Chlamidia pneumoniae while only 5 percent of non-Alzheimer's brains contained the same bacteria. Read more at....
http://www.usnews.com/usnews/health/briefs/alzheimers_neurological/hb041102.htm
In the case of MS, there is evidence for an association of the disease with chronic bacterial and viral infections. Chmielewska-Badora et al. [10] found that 38.5% of MS patients showed evidence of Borrelia antigens in their blood, whereas other neurological patients carried these antigens in blood at a lower prevalence (19%). Chlamydia pneumoniae has also been found in a subgroup of MS patients [11]. By examining cerebral spinal fluid (CSF) these authors found that 10% of MS patients and 18% of patients with probable MS had Chlamydia infections but none of 56 control patients with other neurological disease were positive [11]. Read more at......
http://www.fibromyalgiasupport.com/library/showarticle.cfm/ID/4243/e/1/T/CFIDS_FM/
...evidence that the bacteria (C. pneumoniae) could be involved in the disease (MS) came from the Subramaniam Sriram’s team at the Vanderbilt University Multiple Sclerosis Center in Nashville, Tenn. He previously reported that 97 percent of MS patients had evidence of C. pneumoniae infection in the central nervous system, compared with only 16 percent in patients with other neurological diseases.
More importantly, Chlamydia antigens precipitated out of the oligoclonal bands. “That’s an amazing result – nobody had been able to do that before and the existence of these bands has been known about for more than 60 years,” Dr. Lenz said.
Now Dr. Lenz and his colleagues have taken the work a stage further. By searching through the chlamydial genome, they found a region coding for a protein fragment that closely resembled the MBP 68-86 region of the myelin protein known to be the main target in EAE. Both peptides were found to activate the T cells that stimulate the encephalitis response, and affected rats showed similar signs of disease. Read more at...
http://www.med.wayne.edu/Scribe/scribe01-02/winter02/a-bacterial%20genomics%20reveals%20ms%20trigger.htm
It has been noted that certain neurological diseases have accompanying gastrointestinal manifestations, particularly constipation and diarrhea. This suggests the possibility that an intestinal microorganism may be the cause of both aspects of the disease. In turn, this implies that appropriate antimicrobial therapy might lead to improvement in both gastrointestinal and the neurological aspects. This has been demonstrated in late onset autism (response has been demonstrated with the administration of oral vancomycin and metronidazole), and there are isolated anecdotal reports of improvement in patients with Alzheimer’s disease, schizophrenia, and Parkinson’s disease. Additional diseases that might have similar pathogenesis include attention deficit hyperactivity disorder (ADHD), depression, bipolar disorder, Whipple’s disease, Tourette’s syndrome, Asperger’s syndrome, and Rhett’s syndrome. Disrupted gut microbial flora can also lead to antimicrobial-associated diarrhea and play a role in irritable bowel syndrome and inflammatory bowel disease (ulcerative colitis and Crohn’s disease).
Read more at....
http://www.vard.org/tts/avail/00-075.htm
Could probiotic preparations containing immune-stimulating species such as L. acidophilus LAFTI strain L10 and B. lactis LAFTI strain B94, which also have the ability to suppress intestinal populations of pathogenic bacteria, be a useful adjunct in the treatment of neurological disorders?
In one study, 90 percent of the brains of Alzheimer's victims contained the pneumonia bacteria, Chlamidia pneumoniae while only 5 percent of non-Alzheimer's brains contained the same bacteria. Read more at....
http://www.usnews.com/usnews/health/briefs/alzheimers_neurological/hb041102.htm
In the case of MS, there is evidence for an association of the disease with chronic bacterial and viral infections. Chmielewska-Badora et al. [10] found that 38.5% of MS patients showed evidence of Borrelia antigens in their blood, whereas other neurological patients carried these antigens in blood at a lower prevalence (19%). Chlamydia pneumoniae has also been found in a subgroup of MS patients [11]. By examining cerebral spinal fluid (CSF) these authors found that 10% of MS patients and 18% of patients with probable MS had Chlamydia infections but none of 56 control patients with other neurological disease were positive [11]. Read more at......
http://www.fibromyalgiasupport.com/library/showarticle.cfm/ID/4243/e/1/T/CFIDS_FM/
...evidence that the bacteria (C. pneumoniae) could be involved in the disease (MS) came from the Subramaniam Sriram’s team at the Vanderbilt University Multiple Sclerosis Center in Nashville, Tenn. He previously reported that 97 percent of MS patients had evidence of C. pneumoniae infection in the central nervous system, compared with only 16 percent in patients with other neurological diseases.
More importantly, Chlamydia antigens precipitated out of the oligoclonal bands. “That’s an amazing result – nobody had been able to do that before and the existence of these bands has been known about for more than 60 years,” Dr. Lenz said.
Now Dr. Lenz and his colleagues have taken the work a stage further. By searching through the chlamydial genome, they found a region coding for a protein fragment that closely resembled the MBP 68-86 region of the myelin protein known to be the main target in EAE. Both peptides were found to activate the T cells that stimulate the encephalitis response, and affected rats showed similar signs of disease. Read more at...
http://www.med.wayne.edu/Scribe/scribe01-02/winter02/a-bacterial%20genomics%20reveals%20ms%20trigger.htm
It has been noted that certain neurological diseases have accompanying gastrointestinal manifestations, particularly constipation and diarrhea. This suggests the possibility that an intestinal microorganism may be the cause of both aspects of the disease. In turn, this implies that appropriate antimicrobial therapy might lead to improvement in both gastrointestinal and the neurological aspects. This has been demonstrated in late onset autism (response has been demonstrated with the administration of oral vancomycin and metronidazole), and there are isolated anecdotal reports of improvement in patients with Alzheimer’s disease, schizophrenia, and Parkinson’s disease. Additional diseases that might have similar pathogenesis include attention deficit hyperactivity disorder (ADHD), depression, bipolar disorder, Whipple’s disease, Tourette’s syndrome, Asperger’s syndrome, and Rhett’s syndrome. Disrupted gut microbial flora can also lead to antimicrobial-associated diarrhea and play a role in irritable bowel syndrome and inflammatory bowel disease (ulcerative colitis and Crohn’s disease).
Read more at....
http://www.vard.org/tts/avail/00-075.htm
Could probiotic preparations containing immune-stimulating species such as L. acidophilus LAFTI strain L10 and B. lactis LAFTI strain B94, which also have the ability to suppress intestinal populations of pathogenic bacteria, be a useful adjunct in the treatment of neurological disorders?
16 January, 2006
Are probiotic yoghurts potent enough to do any good?
The de facto standard for the level of probiotic cells in probiotic yogurts at the end of shelf-life is generally accepted to be in Australia 10^6 (one million) cfu (colony forming units)/g. At the beginning of shelf life, an AB (acidophilus/bifidus) yogurt that meets that standard needs to have around 10^7 cfu/g. The Lactobacillus acidophilus count will then meet the standard at the best before date but the bifido in all likelyhood will not. Bifidobacterium lactis strains will have dropped to around 10^5 cfu/g and if they use human strains such as B. infantis it will have dropped a log or two more, which makes the latter pretty useless.
The de facto standard for the level of probiotic cells in probiotic yogurts at the end of shelf-life is generally accepted to be in Australia 10^6 (one million) cfu (colony forming units)/g. At the beginning of shelf life, an AB (acidophilus/bifidus) yogurt that meets that standard needs to have around 10^7 cfu/g. The Lactobacillus acidophilus count will then meet the standard at the best before date but the bifido in all likelyhood will not. Bifidobacterium lactis strains will have dropped to around 10^5 cfu/g and if they use human strains such as B. infantis it will have dropped a log or two more, which makes the latter pretty useless.
15 January, 2006
Probiotic enemas:
Professor Thomas Borody of the Centre for Digestive Diseases in Five Dock here in Sydney, has patented the use of probiotics in enema format. He has used a probiotic preparation to infuse patients' bowels by the rectal route and has had significant success. Having tried it myself I too found that it gives results that are significantly ahead of those achieved by the oral route. Others have reported the same, positive outcome. A simple device consisting of a 20cc syringe and a piece of silicone tubing suffices as a delivery device. This route has the advantage of bypassing debilitating gastric juices and would presumably also bypass food sensitivity sites in the upper gastro-intestinal tract. This may mean that individuals who are sensitive to ingredients such as the Hi-maize or milk may be able to gain considerable advantage from the probiotics.
Professor Thomas Borody of the Centre for Digestive Diseases in Five Dock here in Sydney, has patented the use of probiotics in enema format. He has used a probiotic preparation to infuse patients' bowels by the rectal route and has had significant success. Having tried it myself I too found that it gives results that are significantly ahead of those achieved by the oral route. Others have reported the same, positive outcome. A simple device consisting of a 20cc syringe and a piece of silicone tubing suffices as a delivery device. This route has the advantage of bypassing debilitating gastric juices and would presumably also bypass food sensitivity sites in the upper gastro-intestinal tract. This may mean that individuals who are sensitive to ingredients such as the Hi-maize or milk may be able to gain considerable advantage from the probiotics.
13 January, 2006
Auto-immune diseases and Leaky gut syndrome.
The model for the cause of auto-immune diseases (and there are at least 130 of them) is quite straight forward. Firstly there has to be a genetic predispostion. This simply means that a gene is present (or more precisely a form of a normal gene) that is recognised by the antibodies that cause the disease. Thus in Rheumatoid Arthritis the RA gene encodes for a particular variant of a normal structural protein in the joints. But the presence of the gene alone is not sufficient to cause the disease. Genetically engineered mice that have the human RA gene in their DNA and have been delivered by aseptic caesarian and kept germ-free do not develop the disease. But if bacteria are introduced to their gut they develop arthritis.
But how do the bacteria trigger the formation of the antibodies? Firstly it needs to be understood that the inside of intestines are contiguous with the outside of our bodies and are, technically speaking, not on our "insides". Our true insides lie the other side of the intestinal wall and bacteria are looking for ways to make that journey. There are more than 10 mechanisms that have been identified whereby various bacteria facilitate translocation of themselves into our true interior. For example, we produce a protein called zonulin which we use to regulate the permeability of our intestinal wall. It operates on the tight junctions (the so-called "zonula occludens") which it opens. Normally only small molecules such as simple sugars, minerals and amino acids, etc., are transported through or diffuse through the cell walls. Interestingly, people with celiac disease are genetically programmed to produce 15 times too much zonulin and this makes their intestines permeable to large molecules such as gluten. Some bacteria can produce a protein that mimics zonulin, in fact the last 20 amino acids are identical. This bacterial "zonulin" opens the tight junctions and the bacterium can slip on through. Once on the inside, it provokes an immune response. The bacterial cells are killed and their contents are spilled out. Inside, the bacteria have many structures that resemble our own and when antibodies are made to these, these same antibodies can react with any human structures that they "recognise".
RA and SLE (lupus) both involve overgrowth of the small intestine with E. coli and perhaps other Gram negative bacteria are involved in other conditions. Yersinia is thought to be involved in Ankylosing Spondylitis, for example.
The antibodies of SLE have been found to cross-react with the lac7 gene in E. coli, suggesting that this is the trigger.
The model for the cause of auto-immune diseases (and there are at least 130 of them) is quite straight forward. Firstly there has to be a genetic predispostion. This simply means that a gene is present (or more precisely a form of a normal gene) that is recognised by the antibodies that cause the disease. Thus in Rheumatoid Arthritis the RA gene encodes for a particular variant of a normal structural protein in the joints. But the presence of the gene alone is not sufficient to cause the disease. Genetically engineered mice that have the human RA gene in their DNA and have been delivered by aseptic caesarian and kept germ-free do not develop the disease. But if bacteria are introduced to their gut they develop arthritis.
But how do the bacteria trigger the formation of the antibodies? Firstly it needs to be understood that the inside of intestines are contiguous with the outside of our bodies and are, technically speaking, not on our "insides". Our true insides lie the other side of the intestinal wall and bacteria are looking for ways to make that journey. There are more than 10 mechanisms that have been identified whereby various bacteria facilitate translocation of themselves into our true interior. For example, we produce a protein called zonulin which we use to regulate the permeability of our intestinal wall. It operates on the tight junctions (the so-called "zonula occludens") which it opens. Normally only small molecules such as simple sugars, minerals and amino acids, etc., are transported through or diffuse through the cell walls. Interestingly, people with celiac disease are genetically programmed to produce 15 times too much zonulin and this makes their intestines permeable to large molecules such as gluten. Some bacteria can produce a protein that mimics zonulin, in fact the last 20 amino acids are identical. This bacterial "zonulin" opens the tight junctions and the bacterium can slip on through. Once on the inside, it provokes an immune response. The bacterial cells are killed and their contents are spilled out. Inside, the bacteria have many structures that resemble our own and when antibodies are made to these, these same antibodies can react with any human structures that they "recognise".
RA and SLE (lupus) both involve overgrowth of the small intestine with E. coli and perhaps other Gram negative bacteria are involved in other conditions. Yersinia is thought to be involved in Ankylosing Spondylitis, for example.
The antibodies of SLE have been found to cross-react with the lac7 gene in E. coli, suggesting that this is the trigger.
11 January, 2006
A model for "the cause of 'everything'" is hereby proposed.
"Everything" is in inverted commas for obvious reasons, but the about 1.5kg of bacteria that reside in our intestines is a potent producer of enzymes and other compounds, many of which have the capacity to do us significant damage. And the approximately 1000 species of bacteria that this represents are different for each individual. This produces a wide range of potentially negative (and many positive) outcomes, especially when superimposed against the varied genetic backgrounds of the hosts.
Back in the mid 1970's I had a discussion with Dr. William Murrell (a research scientist at CSIRO). He was investigating the mechanisms behind Sudden Infant Death Syndrome (SIDS). He found that the intestines of SIDS victims were full of spore-forming bacteria (Clostridia and Bacillus species). When he cultured these bacteria and put them into the intestines of rabbits, the rabbits "just went to sleep and died". He postulated that SIDS was caused by the presence of bacterial neurotoxins in sufficient quantities to affect the nerves that control breathing and that this is what caused their death.
If one puts "tetanus + autism" into Google, one gets 222,000 hits. One of the most interesting theories of what causes autism is that Clostridium tetani, the bacterium that causes tetanus, is present in the intestines of autistic children. These children test positive for the presence of antibodies to the neurotoxin produced by Cl. tetani, indicating that they have been exposed to it. When treated with antibiotics, autistic children respond dramatically but then revert once treatment stops. The theory is that the organism gets into the child's intestine while the immune system is still "learning" to distinguish friendly gut microbes from unfriendly ones. This leads to a tolerance of that bacterium and a the immune system fails to "kick it out" of the intestine. The neurotoxin travels from the intestine up the vagus nerve to the brain where it inhibits the production of neurotransmitters such as serotonin and possibly also acts as a vasoconstrictor and restricts the blood supply to the temporal lobes of the brain.
More next time.
"Everything" is in inverted commas for obvious reasons, but the about 1.5kg of bacteria that reside in our intestines is a potent producer of enzymes and other compounds, many of which have the capacity to do us significant damage. And the approximately 1000 species of bacteria that this represents are different for each individual. This produces a wide range of potentially negative (and many positive) outcomes, especially when superimposed against the varied genetic backgrounds of the hosts.
Back in the mid 1970's I had a discussion with Dr. William Murrell (a research scientist at CSIRO). He was investigating the mechanisms behind Sudden Infant Death Syndrome (SIDS). He found that the intestines of SIDS victims were full of spore-forming bacteria (Clostridia and Bacillus species). When he cultured these bacteria and put them into the intestines of rabbits, the rabbits "just went to sleep and died". He postulated that SIDS was caused by the presence of bacterial neurotoxins in sufficient quantities to affect the nerves that control breathing and that this is what caused their death.
If one puts "tetanus + autism" into Google, one gets 222,000 hits. One of the most interesting theories of what causes autism is that Clostridium tetani, the bacterium that causes tetanus, is present in the intestines of autistic children. These children test positive for the presence of antibodies to the neurotoxin produced by Cl. tetani, indicating that they have been exposed to it. When treated with antibiotics, autistic children respond dramatically but then revert once treatment stops. The theory is that the organism gets into the child's intestine while the immune system is still "learning" to distinguish friendly gut microbes from unfriendly ones. This leads to a tolerance of that bacterium and a the immune system fails to "kick it out" of the intestine. The neurotoxin travels from the intestine up the vagus nerve to the brain where it inhibits the production of neurotransmitters such as serotonin and possibly also acts as a vasoconstrictor and restricts the blood supply to the temporal lobes of the brain.
More next time.
09 January, 2006
Probiotic + Prebiotic = Synbiotic:
The combination of the good cultures and the "packed lunch" that will sustain them on their journey through the gastro-intestinal tract is termed a synbiotic product. As a rough rule of thumb, prebiotics on their own do more than probiotics do on their own when it comes to alleviating overt symptoms of gastro-intestinal disturbance. The combination of the two is, however, much more powerful than either alone.
The combination of the good cultures and the "packed lunch" that will sustain them on their journey through the gastro-intestinal tract is termed a synbiotic product. As a rough rule of thumb, prebiotics on their own do more than probiotics do on their own when it comes to alleviating overt symptoms of gastro-intestinal disturbance. The combination of the two is, however, much more powerful than either alone.
08 January, 2006
Prebiotics are important.
An army travels on its stomach. Prebiotics are fibre compounds that resist digestion and absorption by the enzymes in our small intestines. When they reach the large intestine they are digested by many of the "good" bacteria that are there. In the case of Hi-maize resistant starch, the starch granules also act as a protective transport medium as the probiotic cells adsorb to them. This helps to boost the numbers of probiotic cells that reach the colon. CSIRO experiments by Dr A. Bird et. al., showed that combining fructo-oligosacharide and Hi-maize boosted the numbers of probiotic cells that reached the far end of the colon by almost 50-fold.
An army travels on its stomach. Prebiotics are fibre compounds that resist digestion and absorption by the enzymes in our small intestines. When they reach the large intestine they are digested by many of the "good" bacteria that are there. In the case of Hi-maize resistant starch, the starch granules also act as a protective transport medium as the probiotic cells adsorb to them. This helps to boost the numbers of probiotic cells that reach the colon. CSIRO experiments by Dr A. Bird et. al., showed that combining fructo-oligosacharide and Hi-maize boosted the numbers of probiotic cells that reached the far end of the colon by almost 50-fold.
07 January, 2006
Numbers matter. A war is going on in our intestines. We often hear that we are 90% bacteria and 10% human on the basis of cell numbers. There are 90 trillion bacteria in our intestines and they are producing more bio-active compounds than our livers! We could be viewed simply as walking fermenters, full of bacteria, all striving for the upper hand. Many people who are suffering from disorders related to a "sick" bowel microflora are told that they're suffering from stress or are imagining their symptoms: The medical profession as a whole seems to be ill-prepared to handle the new pandemics of metabolic diseases that afflict so many. In theory, probiotics offer a way to combat these disorders by getting at the cause rather than trying to treat the symptoms. But traditional probiotic products have suffered from a number of short-comings that have meant that the possibilities have been discounted. Firstly they have been made up of poorly-selected strains. Secondly, the numbers of cells in these products have been too low to begin with and even lower once they have been stored for a while. What are a billion cells or less going to do against 90 trillion intestinal bacteria? Numbers of probiotic cells do matter and need to be up in the trillions before they can hope to show an effect against the bacteria that are causing disease symptoms. More to come.
06 January, 2006
Important characteristics of an effective probiotic product.
1. Strain characteristics.
An effective probiotic strain needs to be able to suppress undesirable bacteria. Many acidophilus strains on the market actually do the opposite! Lactobacillus acidophilus LAFTI strain L10 was selected for its activity against pathogens such as E. coli, Listeria and Salmonella.
It is also desirable that the strains are able to attach to the lining of the intestine and remain in the gastro-intestinal tract for as long as possible. It is also desirable that the strains used can positively stimulate the immune system. Both L10 and Bifidobacterium lactis LAFTI strain B94 do this. L10 is also known to reduce allergic reactions.
It is also important that the strains used are able to survive for as long as possible and multiply in the intestine. Both B94 and L10 have been shown to be more effective than other strains at doing this.
More important characteristics next time.
1. Strain characteristics.
An effective probiotic strain needs to be able to suppress undesirable bacteria. Many acidophilus strains on the market actually do the opposite! Lactobacillus acidophilus LAFTI strain L10 was selected for its activity against pathogens such as E. coli, Listeria and Salmonella.
It is also desirable that the strains are able to attach to the lining of the intestine and remain in the gastro-intestinal tract for as long as possible. It is also desirable that the strains used can positively stimulate the immune system. Both L10 and Bifidobacterium lactis LAFTI strain B94 do this. L10 is also known to reduce allergic reactions.
It is also important that the strains used are able to survive for as long as possible and multiply in the intestine. Both B94 and L10 have been shown to be more effective than other strains at doing this.
More important characteristics next time.
04 January, 2006
27/06/2002 - Probiotics or ‘friendly’ bacteria given to babies during weaning may help alleviate the symptoms of eczema, according to research published in the British journal Gut.
Read more at http://www.nutraingredients.com/news/listnews.asp?m=5&y=2005
Read more at http://www.nutraingredients.com/news/listnews.asp?m=5&y=2005
03 January, 2006
Colicky Babies and Probiotics
http://www.ingentaconnect.com/content/tandf/spae/2004
Intestinal microflora in breastfed colicky and non-colicky infants
Authors: F Savino1; F Cresi1; S Pautasso1; E Palumeri1; V Tullio2; J Roana2; L Silvestro1; R Oggero1
Source: Acta Paediatrica, Volume 93, Number 6, June 2004, pp. 825-829(5)
Publisher: Taylor and Francis Ltd
Abstract:
Background: Infantile colics are a common problem in the first months of life. During this period, a process of intestinal colonization rapidly occurs. A difference in the gut microflora could play an important role in the pathogenesis of colics, changing the metabolism of carbohydrates and fatty acids. Actually, in the literature, only few data have been collected about this topic. In this study, we evaluated intestinal microflora in breastfed colicky and non-colicky infants. Methods: Seventy-one breastfed infants, aged 3.2 ± 0.6 wk, free from episodes of gastroenteritis and without previous assumption of antibiotic and probiotic drugs, were enrolled in the study. They were divided into two groups: colicky (42 cases) and non-colicky (29 cases), according to Wessel's criteria. Stool samples were collected, diluted and cultured on several selective media to detect lactobacilli, clostridia, Gram-negative anaerobes and Enterobacteriaceae. Statistical analysis was performed using Student's t-test, 2 test and a non-parametric test (Mann-Whitney U-test). Results: Differences in gut microflora were found among colicky and non-colicky infants: colicky infants were less frequently colonized by Lactobacillus spp., and more frequently by anaerobic Gram-negative bacteria.
Conclusion: Our study indicates that colicky infants have different patterns of gut microflora. Further studies are required to understand whether gut microflora is the primary cause of colics or its consequence.
Keywords: Breastfed infants; infantile colic; lactobacilli; microflora
Document Type: Research article
DOI: 10.1080/08035250410027625
Affiliations: 1: Department of Paediatrics University of Turin Turin Italy 2: Department of Public Health and Microbiology University of Turin Turin Italy
http://www.ingentaconnect.com/content/tandf/spae/2004
Intestinal microflora in breastfed colicky and non-colicky infants
Authors: F Savino1; F Cresi1; S Pautasso1; E Palumeri1; V Tullio2; J Roana2; L Silvestro1; R Oggero1
Source: Acta Paediatrica, Volume 93, Number 6, June 2004, pp. 825-829(5)
Publisher: Taylor and Francis Ltd
Abstract:
Background: Infantile colics are a common problem in the first months of life. During this period, a process of intestinal colonization rapidly occurs. A difference in the gut microflora could play an important role in the pathogenesis of colics, changing the metabolism of carbohydrates and fatty acids. Actually, in the literature, only few data have been collected about this topic. In this study, we evaluated intestinal microflora in breastfed colicky and non-colicky infants. Methods: Seventy-one breastfed infants, aged 3.2 ± 0.6 wk, free from episodes of gastroenteritis and without previous assumption of antibiotic and probiotic drugs, were enrolled in the study. They were divided into two groups: colicky (42 cases) and non-colicky (29 cases), according to Wessel's criteria. Stool samples were collected, diluted and cultured on several selective media to detect lactobacilli, clostridia, Gram-negative anaerobes and Enterobacteriaceae. Statistical analysis was performed using Student's t-test, 2 test and a non-parametric test (Mann-Whitney U-test). Results: Differences in gut microflora were found among colicky and non-colicky infants: colicky infants were less frequently colonized by Lactobacillus spp., and more frequently by anaerobic Gram-negative bacteria.
Conclusion: Our study indicates that colicky infants have different patterns of gut microflora. Further studies are required to understand whether gut microflora is the primary cause of colics or its consequence.
Keywords: Breastfed infants; infantile colic; lactobacilli; microflora
Document Type: Research article
DOI: 10.1080/08035250410027625
Affiliations: 1: Department of Paediatrics University of Turin Turin Italy 2: Department of Public Health and Microbiology University of Turin Turin Italy
02 January, 2006
Why do some people have an immune response to themselves and to some foods?
Recently, a paper was published that announced the discovery, in the human intestine, of a human protein that the researchers called “Zonulin”. Zonulin controls the strength of the normally tight junctions between the cells that make up the wall of the intestine. The more zonulin there is, the more permeable the intestine becomes. The name derives from a bacterium called "Zonula occludens" which was found to produce a protein that mimics the action of the human one. It could be that the presence of a similar bacterium in the gut is actually the cause of "leaky gut" syndrome. One experiment showed that the presence of high numbers of E. coli in the colon, was associated with the production of large amounts of zonulin, thereby opening up the junctions and allowing the passage of the E. coli through the intestinal wall (a phenomenon called “translocation”) and into the blood. A food substance called inulin (which is basically lots of fructose molecules joined in chains) was added to the diet and tests of the subjects’ urine revealed that this too had been translocated. It is known that the presence of any large molecules or bacteria in the blood stream will elicit the production of antibodies to fight the perceived invaders. These same researchers then added a probiotic organism (a Lactobacillus) to the patients’ diet and were able to demonstrate that it reduced the translocation of E. coli cells and inulin by up to 100-fold. It is tempting to assume that, given the body’s ability to recover this should also reduce the severity of any disease that is being triggered in this way.
Recently, a paper was published that announced the discovery, in the human intestine, of a human protein that the researchers called “Zonulin”. Zonulin controls the strength of the normally tight junctions between the cells that make up the wall of the intestine. The more zonulin there is, the more permeable the intestine becomes. The name derives from a bacterium called "Zonula occludens" which was found to produce a protein that mimics the action of the human one. It could be that the presence of a similar bacterium in the gut is actually the cause of "leaky gut" syndrome. One experiment showed that the presence of high numbers of E. coli in the colon, was associated with the production of large amounts of zonulin, thereby opening up the junctions and allowing the passage of the E. coli through the intestinal wall (a phenomenon called “translocation”) and into the blood. A food substance called inulin (which is basically lots of fructose molecules joined in chains) was added to the diet and tests of the subjects’ urine revealed that this too had been translocated. It is known that the presence of any large molecules or bacteria in the blood stream will elicit the production of antibodies to fight the perceived invaders. These same researchers then added a probiotic organism (a Lactobacillus) to the patients’ diet and were able to demonstrate that it reduced the translocation of E. coli cells and inulin by up to 100-fold. It is tempting to assume that, given the body’s ability to recover this should also reduce the severity of any disease that is being triggered in this way.
01 January, 2006
It is highly probable that allergic conditions such as asthma, hay fever and dermatitis are triggered by undesirable bacteria binding to receptors called Peyer's Patches in the small intestine. Regular consumption of Lactobacillus acidophilus LAFTI strain L10 seems to displace these bacteria and, unlike many acidophilus strains, L10 has the ability to combat such conditions. See also the following abstract at http://www.findarticles.com/p/articles/mi_m0FDN/is_6_6/ai_81761469
Allergy development and the intestinal microflora during the first year of life - Abstract
Alternative Medicine Review, Dec, 2001
BACKGROUND: The intestinal microflora is a likely source for the induction of immune deviation in infancy. OBJECTIVE: The purpose of this study was to prospectively relate the intestinal microflora to allergy development in 2 countries differing with respect to the prevalence of atopic diseases. METHODS: Newborn infants were followed prospectively through the first 2 years of life in Estonia (n = 24) and Sweden (n = 20). By that age, 9 Estonian and 9 Swedish infants had developed atopic dermatitis and/or positive skin prick test results. Stool samples were obtained at 5 to 6 days and at 1, 3, 6, and 12 months, and 13 groups of aerobic and anaerobic microorganisms were cultivated through use of standard methods. RESULTS: In comparison with healthy infants, babies who developed allergy were less often colonized with enterococci during the first month of life (72% vs 96%; P <.05) and with bifidobacteria during the first year of life (17% to 39% vs 42% to 69%; P <.05). Furthermore, allergic infants had higher counts of clostridia at 3 months (median value, 10.3 vs 7.2 log(10); P <.05). The prevalence of colonization with Staphylococcus aureus was also higher at 6 months (61% vs 23%; P <.05), whereas the counts of Bacteroides were lower at 12 months (9.9 vs 10.6 log(10); P <.05). CONCLUSION: Differences in the composition of the gut flora between infants who will and infants who will not develop allergy are demonstrable before the development of any clinical manifestations of atopy. Because the observations were made in 2 countries with different standards of living, we believe that our findings could indicate a role for the intestinal microflora in the development of and protection from allergy.
Bjorksten B, Sepp E, Julge K, et al. J Allergy Clin Immunol 2001;108:516-520.
Allergy development and the intestinal microflora during the first year of life - Abstract
Alternative Medicine Review, Dec, 2001
BACKGROUND: The intestinal microflora is a likely source for the induction of immune deviation in infancy. OBJECTIVE: The purpose of this study was to prospectively relate the intestinal microflora to allergy development in 2 countries differing with respect to the prevalence of atopic diseases. METHODS: Newborn infants were followed prospectively through the first 2 years of life in Estonia (n = 24) and Sweden (n = 20). By that age, 9 Estonian and 9 Swedish infants had developed atopic dermatitis and/or positive skin prick test results. Stool samples were obtained at 5 to 6 days and at 1, 3, 6, and 12 months, and 13 groups of aerobic and anaerobic microorganisms were cultivated through use of standard methods. RESULTS: In comparison with healthy infants, babies who developed allergy were less often colonized with enterococci during the first month of life (72% vs 96%; P <.05) and with bifidobacteria during the first year of life (17% to 39% vs 42% to 69%; P <.05). Furthermore, allergic infants had higher counts of clostridia at 3 months (median value, 10.3 vs 7.2 log(10); P <.05). The prevalence of colonization with Staphylococcus aureus was also higher at 6 months (61% vs 23%; P <.05), whereas the counts of Bacteroides were lower at 12 months (9.9 vs 10.6 log(10); P <.05). CONCLUSION: Differences in the composition of the gut flora between infants who will and infants who will not develop allergy are demonstrable before the development of any clinical manifestations of atopy. Because the observations were made in 2 countries with different standards of living, we believe that our findings could indicate a role for the intestinal microflora in the development of and protection from allergy.
Bjorksten B, Sepp E, Julge K, et al. J Allergy Clin Immunol 2001;108:516-520.
