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Posted by Gut Microflora on April 14, 2002 at 15:41:53:

Autism and the Human Gut Microflora


Max Bingham


Food Microbial Sciences Unit


Science and Technology Centre, Earley Gate, University of Reading, Whiteknights Road, Reading, Berkshire, UK. RG6 6BZ

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Contents

Introduction
Gut Microbiology
Factors affecting the Human Gut Microflora
Antibacterial Drugs
Age as a factor affecting the Gut Microflora
The Autistic Human Gut Microflora
Candida spp
The Herxheimer Reaction
Considerations of Gluten and Casein Removal
Clostridia and Autism
Sulphate Reducing Bacteria
Dermorphin and Deltorphin
Treatments
Probiotics, Prebiotics and Synbiotics
Probiotics
The alternative approach - prebiotics
Synbiotics
Relevance to Autistic Symptoms
On going research at Reading
Summary
References
Introduction

Research to date has suggested that there may be a link between the development of autistic symptoms and an abnormal human gut microflora. It has been shown previously, that autistic subjects tend to exhibit an elevated level of yeasts (particularly Candida spp) (Shaw, Kassen & Chaves, 1995) and/or certain gut anaerobes in their lower intestines. Other reports have suggested that the onset of certain Autistic Spectrum Disorders may be related to the occurrence of otitis media (ear infections) (Kontstantareas & Homatidis, 1987) or maybe other typical childhood illnesses. It is common to treat this sort of infection with some sort of broad-spectrum antibiotic. Intestinal overgrowth of yeast and certain anaerobic bacteria are a well documented outcome of administration of broad spectrum antibiotics (Kennedy & Volz, 1983; Danna et al, 1991; Ostfield et al, 1977; Kinsman et al, 1989; Van der Waaij, 1987; Samsonis et al, 1993, 1994a,b).

While the onset of otitis media/ other childhood illnesses and the occurrence of a yeast/ selected gut anaerobe overgrowth may not be the cause of autistic symptoms, it appears there may be a link. Products of the human gut microflora in relation to autism and its symptoms appear to have been largely ignored in the past. However they appear to be relevant certainly in terms of yeast species and certain gut anaerobes.

This report will outline the currently available evidence for a possible link between the development of autistic symptoms and abnormal human gut microflora. It will consider the roles species may take in this development and consider methods currently available that may help treat these abnormalities and as a result help alleviate the severity of some symptoms seen in autism.

Gut Microbiology at Reading

Research at the Food Microbial Sciences Unit utilises expertise in gut microbiology, anaerobic bacteriology and molecular biology to reliably identify species and systems involved in a wide variety of applications. The Human Gut Microflora is an extremely complex mixed culture comprising mainly of bacteria living in a state of dynamic equilibrium. It is estimated that as many as 500 different species reside in the colon at any one time. In the small intestine and stomach much lower numbers can be found (Figure 1).


Figure 1: Location of the Human Gut Microflora

The colon is regarded as one of the most metabolically active sites in the human body and this is due to the human gut microflora. Until recently, research on the human gut microflora has been limited by the fact that only about 88% of cells observed under the microscope are cultureable. A much smaller number are easily cultureable. More recently, the use of molecular based techniques such as DNA extraction and sequencing has meant research can be extended into areas that were previously not possible.



Figure 2: A micrograph of human faeces showing various bacteria and food particles

Figure 3: The major groups of bacterial species found in the human gut with some functions described

Figure 4: The alternative view of the human gut microflora

Factors affecting the Human Gut Microflora

The population of bacteria in the gastro-intestinal tract is determined by a great variety of factors. The most important of these factors are drugs, disease, age and diet. The consequences of these factors may be wide and varied. Figure 5 shows many of the factors.


Figure 5: Factors affecting the Human Gut Microflora (Adapted from Mallet and Rowland, 1988)

Antibacterial Drugs

The use of antibiotics, particularly via the oral route, often results in the suppression of some, though not all, components of the human gut microflora. This suppression will depend upon the antibiotic used and partly on the resistance of the bacteria in the gut. Once established, the gut microflora exhibits a remarkable stability in terms of a dynamic equilibrium. It is a major factor in preventing the establishment of potentially pathogenic or exogenous organisms. This is colonisation resistance. This factor can be significantly disrupted through the use of antibiotics. The strictly anaerobic components of the microflora appear to be the most crucial to the maintenance of colonisation resistance (Van der Waaij, 1979)

Age as a factor affecting the Gut Microflora

At birth the gut exhibits sterility but becomes rapidly colonised by microorganisms passed from the mother and from the environment. Lactobacillus spp and Bifidobacterium spp reach high numbers initially. Shortly after birth, facultative anaerobes such as Streptococcus spp and E.coli can be detected. This population remains fairly stable during suckling. With the introduction of solid food, major changes occur as strict anaerobes such as Bacteroides spp gain supremacy. These changes may significantly affect the susceptibility of the infant to foreign substances. Any disruption to the gut microflora might therefore affect the development of the child. The use of antibiotics could affect this balance of gut microflora.

The Autistic Human Gut Microflora

Many autistic subjects exhibit a range of gut disorders. These can include diarrhoea, constipation, gas retention and abnormal faeces. Imbalances in the gut microflora may be responsible for these problems. Research into the characteristics of the autistic human gut microflora has been extremely limited. It now seems increasingly likely that imbalances in the gut microflora and the development of autistic symptoms may be linked. Certain unusual species of microorganisms may be implicated. These include certain yeasts (Candida spp), certain clostridia may be important and most recently it is thought that sulphate reducing bacteria could be included in this list. Controlling the growth of these organisms may help to alleviate some symptoms of autism.

Candida spp

Candida normally constitutes only a very small proportion of the human gut microflora. Competitive inhibition and certain immune functions keep growth under control. Previous research has led some groups to suggest that certain autistic characteristics may partially be a consequence of an overgrowth of Candida spp. Elevated yeast metabolites such as tartaric acid and arabinose appear to be relatively common in autism. The arabinose appears to be involved in abnormal protein binding which may adversely affect neuron connection and this may have relevance to the appearance of autistic symptoms (Sell & Monnier, 1989; Shaw et al, 1999). Given the intolerance that autistic subjects appear to have to gluten and casein, an involvement of arabinose and pentosidine formation may be important. However the exact biochemical role of arabinose remains unclear.

Tartaric acid from a yeast overgrowth may have a direct toxic effect on muscles and is a key inhibitor of the Krebs cycle that supplies raw materials for gluconeogenesis (Shaw, Cassen & Chaves, 1995). The implications of this appear to be detrimental to autistic function. Furthermore, it has been shown that Candida albicans can produce gliotoxins (Shah & Larsen, 1991, 1992) and immunotoxins (Podorski et al, 1989; Witken, 1985), which may have further relevance to the development of autisitic symptoms.

Over 160 species of Candida have been identified (Barnett et al, 1990). They are described as ovoid budding yeasts that typically reproduce vegetatively and may exhibit hyphae. Figures 6 and 6a are micrographs demonstrating certain characteristics of Candida.

Figure 6: An ovoid budding Candida cell. Micrograph from http://research.amnh.org/exhibitions/epidemic/microbes.html

Figure 6a: Candia exhibiting hyphae and reproducing vegetatively
http://www.medsch.wisc.edu/medmicro/myco/Images/c_albicans.html

Six Candida species have been implicated as human pathogens. Candida albicans and Candida tropicalis are thought to cause the majority of Candida infections. Clinical manifestations of a Candida overgrowth vary widely but can include fatigue, mood lability, depression, inability to concentrate, headaches, loss of energy, food cravings, mould sensitivity and multiple food and chemical intolerances. In children, chronic recurrent infections are common and these often require antibiotics. Carbohydrate cravings and central nervous system dysfunction are also seen (Kroker, 1987).

Candida albicans may interfere with immune function at a number of levels. This can include interfence with correct Candida antigen presentation by macrophages; secretion of hyphal substances; subsequent release of by-products and toxins into circulation and this generalised impairment in cellular immunity may encourage further development of Candida colonisation.

The metabolic and toxic potential of Candida albicans includes the capacity to produce multiple toxins. Many yeast organisms can metabolise sugars to pyruvate and this in turn is anaerobically converted to acetaldehyde and carbon dioxide. Chronic CO2 production may account for the persistent bloating and gas noted clinically by many patients with chronic candidiasis. Some strains of Candida can reduce acetaldehyde to ethanol. This would be rapidly absorbed and contribute to a raised blood alcohol level and state of chronic alcohol intoxication can ensue. It may be that chronic acetaldehyde production is important. Truss (1984) proposes that this may be responsible for multiple central nervous system dysfunctions through:

Acetaldehyde induced loss of red blood cell flexibility with resultant diminished oxygen tissue delivery.
Acetaldehyde binding to amine groups of neurotransmitters.
Acetaldehyde oxidation leading to a chronically elevated NADH/NAD ratio with multiple potential neuronal metabolic problems.
Vitamin deficiencies are commonly seen with a Candida overgrowth. Lowered vitamin B6 and B2 are most often seen. This could conceivably contribute to multiple symptoms including fatigue, depression, neuropathic problems, heightened oedema formation and additional metabolic dysfunction.

Clinical expression of fatty acid deficiency is often seen in-patients with candidiasis. Galland (1985) reported nearly 66% of candidiasis patients he studied had two or more clinical signs of fatty acid deficiency. Non-specific signs such as dry stiff hair, dry scaly skin, brittle nails and follicular dermatitis where noted in many of these patients.

Figure 7: A model of Candidiasis (adapted from Kroker, 1987)

Shaw et al (1999) speculated that many of the symptoms of autism might be related to an overgrowth of Candida and a selective IgA deficiency. Treatment with anti-fungal drugs and a gluten and casein free diet led to the improvement in symptoms seen in a severely autistic child. In further work Shaw (1999) was able to show that children exhibiting autistic features have increased excretion of abnormal metabolites (citramalic, tartaric and 3-oxoglutaric acids). It was speculated the source of these might be yeasts. Gas Chromatograpy/ Mass Spectrometry was used to evaluate the urinary content of metabolites on autistic subjects following the administration of Nystatin. Urinary tartaric acid declined to zero after 60 days. Associated changes included improvement in eye contact, a reduction in hyperactivity and an improvement in sleep patterns. When Nystatin dose was cut to half, levels rose and the improvement regressed.

The Herxheimer Reaction

Following the start of anti-fungal treatment, patients often exhibit a transient worsening of symptoms. Values for microbial metabolites often increase dramatically during the immediate period. However levels then fall after 4 days to two weeks. This is a systemic reaction due to the rapid killing of yeast and the consequent absorption of large quantities of fragmented yeast products.

Considerations of gluten and casein removal

It is commonly found that children with autism experience an improvement in symptoms following the removal of these proteins. Many systems have been proposed for the success of this intervention. Certain Candida spp are known to secrete enzymes including phospholipase and proteases. This might have consequences for gut permeability. It is also known that the mycelium and chlamydospore of certain strains are capable of tissue invasion. This would have significant and important consequences for food absorption and digestion. This may be important for autistic symptoms.

Clostridia and Autism

Bolte (1998) outlined the possibilty of a subacute, chronic tetanus infection of the gut as an underlying cause of autism in some individuals. Extensive antibiotic use creates a favourable environment for colonisation by opportunistic pathogens. Clostridium tetani is a ubiquitous anaerobic bacillus known to produce a potent neurotoxin. The normal site of binding for the toxin is the spinal cord. However, the vagus nerve is capable of transporting tetanus neurotoxin, thus providing a route of ascent from the intestinal tract to the central nervous system and thus bypassing the spinal cord. Once in the brain this may disrupt the release of neurotransmitters. This may explain the characteristics of some autistic symptoms

Sulphate Reducing Bacteria

These strictly anaerobic bacteria are spherical, ovoid, rod-shaped, spiral, or vibrioid shaped. They are 0.4 to 3.0 m m in length and occur singly, in pairs or sometimes as aggregates. This group of bacteria has the capacity to reduce sulphate to H2S. These bacteria can metabolise both hydrogen (from the fermentation of other bacteria) and sulphate (from dietary sources). The products are sulphite and/or hydrogen sulphide (H2S). Hydrogen sulphide is a toxic gas with a characteristic smell of rotten eggs.

Sulphation problems in autism have been proposed for many years now. Waring (2001) has shown that around 95% of autistic children have low serum sulphate, about 15% of that found in control children. This is seen as significant since sulphation is required in the inactivation of certain neurotransmitters in the brain involved in the modulation of mood and behaviour. Reduced sulphation also affects the mucin proteins that line the gastrointestinal tract and this finding is linked with increased gut permeability and inflammatory bowel disease.

The important question remains of why autistic children tend to exhibit such low levels of serum sulphate. Waring (2001) outlined the possibility the cytokines, which are peptides produced in inflammatory processes, may be responsible. It was found that autistic children often have high cytokine levels, and this would have the indirect effect of greatly reducing the production of sulphate. Continuing Waring (2001) describes other studies that shown many autistic children excrete high levels of sulphite in the urine.

This raises the possibility that sulphate-reducing bacteria in the gut have a role in this process. These strains of bacteria would have the capacity to reduce levels of sulphate in the gut by metabolising it to H2S and/or sulphite particularly if the population levels are abnormally high. No research has been completed to date and this remains pure speculation. However, it seems inevitable that these bacteria would have some role to play in this process and may therefore be of importance in the development of the symptoms of autism.

Dermorphin and Deltorphin

The concept of a gluten and casein free diet for alleviating the symptoms of autism is accepted now as relevant intervention. However more recent research into this has raised the possibility of a role for dermorphin and deltorphin in autistic symptomology.

In unpublished work, Friedman (2000) has found dermorphin and deltorphin in the urine of autistic children. Dermorphin and deltorphin are compounds which until now had only been found in the skin secretions of certain frogs belonging to the genus Phyllomedusinae. These include poison dart frogs which have been used for their hallucinogenic properties and also for tipping darts to stun targets. These compounds have been estimated to be many times more potent than morphine on a molar basis. Of great interest is the fact that these compounds are only generated on the skin of these frogs when they are in the wild, but not when raised in captivity outside their natural environment. It is possible that these products might be the consequence of a bacteria or fungal organism on the skin. Since dermorphin and deltorphin have been found in urine from autistic children, it is possible that a bacterial species or fungal organisms are responsible for generating such substances. In support of this, the amino acid form is the D enantiomer and therefore of non-human origin.

It has been suggested by Friedman (2000) that autistic children are deficient in dipeptydyl peptidase IV which appears to be responsible for breaking down morphine related peptides in the gut. The absence of this enzyme might be responsible for the failure to break down these opiate peptides. There are two possibilites for this dysfunction - the enzyme is missing or the enzyme is being inhibited. The bacteria responsible for producing these opiates may be present ubiquitously. However, since autistic children are known to have significant gastro-intestinal problems, it might be that dermorphin and deltorphin are absorbed abnormally and affect the central nervous system. We will have to wait for data to be published before this hypothesis can be reviewed and verified. No research has been completed thus far and so this remains somewhat speculative.

Treatments

Many interventions and treatments have been suggested previously. These include pharmacological treatment, dietary interventions, nutritional supports and phytochemical preparations. Many remain unresearched and questionable in terms of their effectiveness.

Approaches towards Candida Infection

Antifungal therapy is an exceedingly important part of treatment. Nystatin or Diflucan are examples of anti-fungal treatment. This will remove the Candida infection but does not affect bacteria in the gut. Nutritional management is required such that food substrates known to stimulate Candida spp are limited in the diet. Since a Candida infection can induce certain nutritional deficiencies, supplementation is often useful.

Approaches towards an overgrowth of gut bacteria outlined above

There are limited possibilities. Antibiotics are about the only option. However, these may not work since some are now resistant to antibiotics. Also, since antibiotics are thought to have been a root cause of many problems, a reoccurrence of infection may be an outcome.

Probiotics, Prebiotics and Synbiotics

It has been speculated that autistic symptoms and imbalances in the human gut microflora may be linked. This raises the possibility that some autistic symptoms may be managed effectively through dietary procedures that target the gut microflora. Reports suggest that these products have been used as part of interventions aimed at alleviating symptoms of autism.

Probiotics

These are a live microbial feed supplement which beneficially affects the host (Fuller, 1989). Examples include lactobacilli and bifidobacteria. Many strains are used including Lactobacillus acidophillus, Lactobacillus caesi Shirota and Bifidobacterium bifidum. The choice of strain and the number of strains used varies considerably between products. Various mechanisms have been proposed for their success including the production of short-chained fatty acids, lowering of gut pH, competition for nutrients, competition for mucosal adhesion sites, production of antimicrobials (bacteriocins), modulation of the immune system, modulation of the human gut microflora and modification of microbial enzyme activities.

However the success of probiotics is seen as limited for a number of reasons. Initially there is a question of survivability in the product. Often the nutritional environment and transportation conditions mean that many cells are non-vialble by the time the product is consumed. Often the products are not aesthetically pleasing i.e. taste, smell and mouth feel are not pleasent. This also raises a question over their use in infants. A major barrier to success is that the bacteria must survive the extreme conditions of the stomach (i.e gastric acid gives a stomach pH of about 2) and the small intestines (where bile and pancreatic secretions mean survival is questionable. The residual population of ingested bacteria then have to compete with the resident bacteria of the large intestine where it is questionable whether such a limited population would survive.

The alternative approach - prebiotics

These are non-digestible food ingredients that selectively stimulate a limited number of bacteria in the colon, to improve host health (Gibson and Roberfroid, 1995)

Figure 8: Characteristics of prebiotic ingredients

Figure 9: The Bifidobacterium Barrier. Activities resulting from promotion of bifidobacteria

Recognised prebiotics in Europe include:

Fructo-oligosaccharides
Lactulose
Trans-oligosaccharides
Prebiotics under evaluation

Soybean oligosaccharides
Lactosucrose
Xylo-oligosaccharides
Isomalto-oligosaccharides
Gluco-oligosaccharides
Second generation prebiotics
Multifunctional prebiotics
Prebiotics are thought to selectively stimulate the beneficial bacteria (e.g. lactobacilli and bifidobacteria) and selectively inhibit non-beneficial organisms that may cause intestinal upset or other gut problems. Importantly, prebiotics can inhibit pathogen colonisation in the gut by competitive inhibition. Some reported health benefits of prebiotics include prevention of gut infections, reduced risk of colon cancer, reduction in cholesterol and blood lipids and increased bioavailability of minerals. Applications for prebiotics include (currently) beverages and fermented milks, health drinks and spreads, infant formulae and weaning foods, cereals, biscuits and food supplements. Table sugar, candy, frozen yoghurt, ready to eat puddings, drinks, vinegar, biscuits, sausages, powdered drinks and chocolate are all typical vehicles for prebiotics in Japan.

Synbiotics

Synbiotics are a combination of probiotics and prebiotics. They may allow for the dual benefits of both applications to be promoted while reducing the limitations. Appropriate prebiotic use should enhance probiotic survival. Much research is currently ongoing and certain products are now available in Europe. Symbalance, enriched yoghurt from the Swiss dairy company Tonilait, was one of the first synbiotics. It contains three probiotic strains and the branded prebiotic Raftiline from Orafti. More recent launches include Jour apres Jour, a UHT skimmed milk enriched with vitamins, trace elements of micronutrients and the branded soluble fiber Actilight from Beghin Meiji Industries. The European Commission's Scientific Committee on Food (SCF) has approved Actilight, made up of fructo-oligosaccharides obtained from beets. It is said to have technical functions similar to sugar, such as water retention; high viscosity; stability at different temperatures; and a stable pH level.

German companies have also been active in developing these synbiotic products. Bauer launched Probiotic Plus Oligofructose, which contains two probiotic strains and the prebiotic, Raftilose. In addition, prebiotics are suitable for a wider application range than probiotics, such as the recently launched Ligne Bifide range from Vivis in France, which includes biscuits, soups and ready meals that contain Actilight.

Relevance to Autistic Symptoms

Recolonisation of the gut with beneficial bacteria is the aim following the removal of pathogenic bacteria (outlined above). Prevention of colonisation by non-beneficial bacteria is necessary. Probiotics may not survive or re-colonise the gut on their own. Prebiotics may help boost their ability to recolonise in the autistic gut. Both (synbiotics) may provide the host with adequate protection from recolonisation by pathogenic microorganisms (such as candida or certain gut anaerobes. A transient improvement in the gut environment may be seen. A transient improvement in autistic symptoms may be seen. The chances of recolonisation by pathogenic bacteria and subsequent relapse of symptoms is reduced.

On going research at Reading

Major themes include, molecular tracking of the human gut microflora, the fermentation process, gastrointestinal health and disease, in-vitro human gut modelling and isolation and development of specific probiotics, prebiotics and synbiotics. Research into autism, until recently, was not an area that the Food Microbial Sciences Unit has been involved with. However, over the past year we have been reviewing on-going research in the area. We now view this as an important area of gut microbiology. We are currently involved with a collaberative research project aimed at characterising about 140 faecal bacterial isolates from autistic children. We have also been investigating the proliferation of Candida species in in vitro human gut models and have been able to isolate and characterise a bacterial species with possible anti-candidal properties. It is hoped that by the end of 2001, the Food Microbial Sciences Unit will be in a position to launch a full research programme looking at the human gut microflora and autism.

Summary

Some autistic symptoms may be the result of unusual gut flora activity. Certain yeast and gut anaerobe species may be responsible. The release of toxins and other unusual metabolites may result in the development of some autistic characteristics. This raises the possibility of managing some symptoms through dietary techniques aimed at the gut microflora. Probiotics, prebiotics and synbiotics may help alleviate the severity of some autistic symptoms.

References

Barnett JA, Payne RW and Yarrow D, (1990). Yeasts: Characterisation and identification (Second edition). Cambridge: Cambridge University Press.

Bolte ER, (1998). Autism and Clostridium tetani. Medical Hypotheses 51(2): 133-144.

Danna P, Urban C, Bellin E and Rahal J, (1991). Role of Candida in pathogenesis of antibiotic associated diarrhoea in elderly patients. Lancet 337: 511-14.

Friedman (2001). Explaination of Diet. At: http://www.gfcfdiet.com/Explanationofdiet.htm

Fuller R, (1989). Probiotics in man and animals. Journal of Applied Bacteriology 66: 365 - 378.

Gibson GR and Roberfroid MB (1995). Dietary Modulation of the human colonic microbiota: Introducing the concept of prebiotics. Journal of Nutrition 125: 1401-1412.

Galland L, (1985). Nutrition and Candidiasis. Journal of Orthomolecular Psychiartry 15: 50 - 60.

Kennedy M and Volz P (1983). Dissemination of yeasts after gastrointestinal inoculation in antibiotic-treated mice. Sabouradia21: 27-33.

Kinsman OS and Pitblado K, (1989). Candida albicans gastrointestinal colonization and invasion in the mouse: effect of antibacterial dosing, antifungal therapy, and immunosuppression. Mycoses 32: 664-74.

Kontstanareas M and Homatidis S, (1987). Ear infections in autistic and normal children. Journal of Autism and Developmental Disorders 17: 585

Kroker GF, (1987). Chronic Candidiasis and Allergy In: Brostoff J and Challacombe SJ (eds). Food Allergy and Intolerance. pp 850 872. London: Bailliere-Tindall.

Mallet AK and Rowland IR, (1988). Factors affecting the Gut Microflora. In: Rowland IR (ed) Role of the Gut Flora in Toxicity and Cancer. London: Academic Press.

Ostfeld E, Rubinstein E, Gazit E and Smetana Z, (1977). Effect of systemic antibiotics on the microbial flora of the external ear canal in hospitalized children. Pediatrics 60: 364-66.

Podzorski R, Herron M, Fast D & Nelson R (1989). Pathogenesis of candidiasis. Immunosuppression by cell wall mannan catabolites. Archives of Surgery 124: 1290-1294.

Samonis G and Dassiou M, (1994a). Antibiotics affecting gastrointestinal colonization of mice by yeasts. Chemotherapy 6: 50-2.

Samonis G, Gikas A and Toloudis P, (1994b). Prospective evaluation of the impact of broad-spectrun antibiotics on the yeast flora of the human gut.
European Journal of Clinical Microbiology & Infectious Diseases 13: 665-7.

Samonis G, Gikas A and Anaissie E, (1993). Prospective evaluation of the impact of broad-spectrun antibiotics on gastrointestinal yeast colonization of humans. Antimicrobial Agents and Chemotherapy 37: 51-53.

Sell D & Monnier V, (1989). Structure elucidation of a senescence cross-link from human extracellular matrix. Implications of pentoses in the aging process. Journal of Biological Chemistry 264: 21597-21602.

Shah D & Larsen B, (1992). Identity of a Candida albicans toxin and its production in vaginal secretions. Medical Science Research 20: 353-355.

Shah D & Larsen B, (1991). Clinical isolates of a yeast produce a gliotoxin-like substance. Mycopathologica 116: 203-208.

Shaw W, Baptist J, Geenens D, (1999). Immunodeficiency, gastrointestinal Candidiasis, wheat and dairy sensitivity, abnormal urinary arabinose and autism: a case study. Unpublished: Great Plains Laboratory, Overland Park, Kansas 66204.

Shaw W, (1999) Role for certain yeast and bacteria byproducts discovered by organic acid testing in the etiology of a wide variety of human diseases. Bulletin of The Great Plains Laboratory. Overland park, KS 66204 (913) 341-8949.

Shaw W, Kassen E and Chaves E, (1995). Increased excretion of analogs of Krebs cycle metabolites and arabinose in two brothers with autistic features. Clinicla Chemistry 41: 1094-1104.

Truss CO (1984). Metabolic abnormalities in patients with chronic candidiasis: the acetaldehyde hypothesis. Journal of Orthomolecular Psychiartry 13: 66-93.

Van der Waaij D, (1979). Colonisation resistance of the digestive tract as a major lead in the selection of antibiotics for therapy. In: New Criteria for antimicrobial therapy - maintenance of digestive tract colonisation resistance (eds D van der Waaij and J Verhoef), pp 271-280. Amsterdam: Excerpta Medica.

Van der Waaij D, (1987). Colonization resistance of the digestive tract--mechanism and clinical consequences. Nahrung31: 507-17.

Waring (2001). Sulphate, sulphation and gut permeability: are cytokines involved? In: The Biology of Autism - Unravelled. Conference proceedings 11th May 2001, Institute of Electrical Engineers, Savoy Place, London.

Witken S (1985). Defective immune responses in patients with recurrent candidiasis. Infections in Medicine May/ June pp 129-132.



Re: Candidiasis (Archive in references.)

Posted by Walt Stoll on April 15, 2002 at 08:37:47:

In Reply to: Candiditis posted by Gut Microflora on April 14, 2002 at 15:41:53:

Thanks, Gut.

Walt

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