This blog is a way of sharing the information and resources that have helped me to recover my son Roo from an Autism Spectrum Disorder. What I have learned is to view our symptoms as the results of underlying biological cause, which can be identified and healed. I say "our symptoms" because I also have a neuro-immune disorder called Myalgic Encephalomyelitis.

And, of course, I am not a doctor (although I have been known to impersonate one while doing imaginative play with my son)- this is just our story and information that has been helpful or interesting to us. I hope it is helpful and interesting to you!


Showing posts with label Gut flora and dysbiosis. Show all posts
Showing posts with label Gut flora and dysbiosis. Show all posts

Monday, June 8, 2026

Brain Research in Autism

Dr Martha Herbert MD PhD, a pediatric neurologist at the Center of Morphometric Analysis, Massachusetts General Hospital, wrote a piece that summed up one of the underlying schisms in the research community that explains a lot of the chaos in the brain research community regarding autism as well as why making sense of this research is the source of many disagreements:

"The positions in the parallel sets of debates tend to cluster into two provisional models, each of which links clinical and research data into a different gestalt.  One model sees autism as a strongly genetic brain-based disorder, with a constant prevalence but a recent increase in awareness that has led to the appearance—but not the reality—of an epidemic. The other model sees autism as a genetically influenced but environmentally modulated condition involving multiple systems of the body, with increased numbers being real and related to changes in environmental factors."

Basically, the disagreement is whether autism is the RESULT of abnormalities in the brain, or whether abnormalities found in the brain are CLUES to a deeper underlying cause that was probably triggered by environmental factors.  If you believe that abnormalities in the brain cause autism, then it makes sense to fish around until you find the abnormalities and then simply identify the genes responsible.  As Dr Herbert so eloquently points out in the above article, this approach has not really lead anywhere.  If you view abnormalities in the brain as the result of deeper, underlying causes- if you view autism as a disorder that affects the brain, as Dr Herbert says, rather than one that is of the brain, finding abnormalities in the brain leads to the conclusion that autism is a whole-body, multi-system disorder.  While there is a component of genetic involvement, it is not in a deterministic way- a saying that you hear over and over in the biomedical world is that "genes load the gun, the environment pulls the trigger".  The above article by Dr Herbert is a good introduction to the basics of the biology of autism, including increased oxidative stress, widespread inflammation (including neuroinflammation), impaired mitochondrial function, impaired detoxification ability, and impaired cellular metabolism.

Autism: a Brain Disorder, or a Disorder that Affects the Brain?  by Martha Herbert
Clinical Neuropsychiatry (2005) 2, 6, 354-379
In this paper, Dr Herbert discusses the ideas presented in the article linked to above in much greater detail.  Additionally, she discusses some of the brain research more specifically and flushes out the implications of the different models in regards to interpretation of the results.

So, keeping in mind that brain research in autism is most useful as one piece of a much larger puzzle, here are some studies that provide some insight.  Studies that find involvement of one or more particular brain region:

Stanford Scientists Successfully Reverse Autism Symptoms in Mice
"Overactivity in the reticular thalamic nucleus was shown to cause autism-like behaviors in mice. Drugs that reduce this activity reversed the symptoms."

Left-hemispheric atypicalities in the primary auditory cortex are associated with language comprehension and social skills in children with Autism Spectrum Disorder
"First, the results revealed a reduction of M200 and altered M200 sensory gating effect in the left auditory cortex in children with ASD. Second, these alterations were related to lower language comprehension skills and higher autistic symptom severity. Finally, altered MEG responses were associated with gray matter thickness reduction as well as abnormal gyrification in the primary auditory cortex in ASD. The study revealed low-level functional and structural atypicalities in children with ASD and their relation to clinical phenotype."

Studies suggesting abnormalities in cortical development:









Sunday, February 7, 2016

Probiotics for Specific Conditions

The book A Mother's Guide To Probiotics has information about which strains of probiotics are suited to which specific health needs and diseases.

Probiotic Advisor is a fee-based service with access to evidence-based information about probiotics.
"ProbioticAdvisor.com provides independent, unbiased, evidence-based information on probiotics, their potential risks, and documented benefits."

Some people may need to reduce or avoid intake of d-lactate producing probiotics, because in some people the d-lactate can build up and cause the person to switch from aerobic to anaerobic respiration (this means the mitochondria produce much less energy).  For more on this read this post from the blog Mommypotamus. (L.acidophilis mainly produces d-lactate).  "Low ATP can affect cognitive function, create feelings of fatigue and impair coordination among other things. More generally, symptoms of D-Lactic acidosis include fatigue, confusion, impaired central nervous system function, impaired coordination, depression, nausea, vomiting, anxiety, anemia, headaches and in extreme cases encephalopathy."  Custom Probiotics has a d-lactate-free formulation.

It is best to avoid strep strains for people with PANDAS as they may trigger a flare.  S. Thermophilus seems to be the most common strep strain and is in many preformulated probiotic products.

There are several blog posts out there with lists of which probiotics are supposed to help certain conditions.  These can be like "cheat sheets" if you trust the blogger.  This is one from The Healthy Home Economist, and this is a list someone posted on a forum that I am intending to research further myself.

The Low Histamine Chef also has a post about probiotics that lower histamine levels and are anti-inflammatory here.  In her post she claims that "L. paracasei probiotic can reverse the gut permeability" and "stress can also cause bacteria to cling to the gastrointestinal tract, but this bacteria was prevented from sticking to the mesenteric lymph nodes (in this study) by a mixture of L. rhamnosus and Lactobacillus helveticus ". She also says that "Lactobacillus plantarum lowers/inhibits tyramine and putrescine but no effect on histamine)" She recommends Bifidobacterium infants, Bifidobacterium longum, Bifidiobacterium breve, and Lactobacillus reuteri.

"The probiotic Lactobacillus rhamnosus (and a few others) down-regulate the IgE and Histamine 4 receptor while also up-regulating anti-inflammatory agents like (IL)-8. In English (to quote a group friend): the probiotic turns down the dial on two important allergy/mast cell cell/histamine receptors, while enhancing the activity of anti-inflammatory agents.

Allergy information (this is not complete):

BioKult may contain traces of soy and milk from the growth medium.
PureEncapsulations ProbioMood contains milk.
Xymogen Probio Defense contains soy and milk (seems to contain some corn)
Standard Process ProSynbiotic contains milk and maltodextrin (probably corn).
Culturelle contains maltodextrin and some products contain artificial colors.
Custom Probiotics *may* be grown on corn.
BioRay products often contain maltodextrin.
Florastor contains milk and some products contain artificial flavors.
Theralac contains milk.
Some Garden of Life products contain oat grass and barley grass, another has banana, milk, and fish.
Threelac contains lemon and yeast.
VSL #3 unflavored has cornstarch.

Pure Encapsulations has a soy and dairy free product called Probiotic 50B.
Pure Encapsulations PureProbiotic (allergen-free)
Seeking Health brand seems to be pretty allergy friendly.
Kirkman brand has many different probiotic products, some are allergy-friendly.
Enzymedica ProBio is free of major allergens and has no fillers.  It does contain several strains that we will be avoiding according to the research in this post.
Jarrow Formulas Jarro-Dophilus® AF Allergen-Free is an inexpensive option (does contain L. Acidophilus)

Specific products that seem to match my own family's needs:

Kirkman CD Biotic
Kirkman Bifido Complex
Kirkman Lactobacillus Duo™ - Hypoallergenic
(contains Lactobacillus rhamnosus, Lactobacillus plantarum)
Thorne Bacillus Coagulans
Pure Encapsulations Lactobacillus Sporogenes (contains rice starch)
Seeking Health Probiota Bifido
Seeking Health Bacillus Coagulans
Seeking Health ProBiota Infant Probiotic Powder (except that it contains L. Casei)
Culturelle dairy and gluten free formula (does contain prebiotics)

Possibly good:
Thorne FloraMend Prime Probiotic (pending research of L. Gasseri)
Jarrow Formulas Ideal Bowel Support 299v (does contain a trace of soy)
Natren Bifido Factor Dairy Free (contains potato and chickpea)

If you're not avoiding acidophilus:
Pharmax HLC Maintenance Probiotic Supplement

Gastrointestinal Health

The use of bacterial spore formers as probiotics.
"Among the large number of probiotic products in use today are bacterial spore formers, mostly of the genus Bacillus. Used primarily in their spore form, these products have been shown to prevent gastrointestinal disorders... Specific mechanisms for how Bacillus species can inhibit gastrointestinal infections will be covered, including immunomodulation and the synthesis of antimicrobials."

Review article: probiotics and prebiotics in irritable bowel syndrome
"A range of probiotics including VSL#3 and L. plantarum 299v enhance (intestinal) barrier function.

Many probiotics including Lactobacillus spp. ferment unabsorbed polysaccharides to generate SCFAs including lactic acid. This acidifies the colonic contents; this acidification inhibits some bacteria and allows others to flourish. Thus 2 × 1010 L. plantarum 299v daily in humans increased acetic, proprionic and butyric acid concentration, while increasing the number of faecal Bifidobacteria spp. and Lactobacillus spp. and reducing the numbers of Clostridia spp.

(S)tress-induced increase in gut permeability and associated visceral hypersensitivity can be inhibited by the probiotic L. paracasei and its soluble products.

Two probiotics, Lactobacillus farciminis, a nitric oxide producing probiotics and L. paracasei NCC2461, have been shown to reduce the increased colonic permeability induced by both partial restraint stress and maternal deprivation (in rats).

(A)dministration of L. rhamnosus to healthy volunteers increased IL-10 secretion and decreased TNF, IL-6 and interferon secretion by peripheral blood mononuclear cells (PBMCs). A similar effect was seen with L. rhamnosus GG, which increases serum IL-10 in atopic children. The probiotic mixture VSL#3 (mixture of .6 × 1010 Lactobacillus spp. (casei, plantarum, acidophilus, delbrueckii ssp. bulgaricus) together with Bifidobacterium (longum,breve and infantis) and one strain of Streptococcus salivarius ssp. thermophilus), which is known to exert an anti-inflammatory effect in pouchitis has also been shown to increase FoxP3 mRNA, a marker of Treg cells.

One relevant study using the Trichinella spiralis mouse model of postinfectious IBS showed that the inhibition of small intestinal contractions seen postinfection was reversed by treatment with L. paracasei, both live and using culture media supernatant. A proteomic analysis showed that supernatant treatment normalized a number of proteins related to cytoskeletal organization and stress response and also reduced a number of markers of inflammation.

E. coli Nissle 1917 has been shown to inhibit the visceral hypersensitivity associated with trinitrobenzene sulphonic acid (TNBS) colitis and L. paracasei inhibits the visceral hypersensitivity associated with inflammation in healthy mice in whom the bacterial microbiota have been disturbed by antibiotics.

An entirely novel mode of action of probiotics has recently been demonstrated in which L. acidophilus increased the expression of μ-opioid and cannabinoid receptors in normal animals, a phenomenon which was associated with an inhibition of visceral sensitivity equivalent to that of morphine 0.1 mg/kg. This action appears independent of an anti-inflammatory effect.

Along with colonization of the gut, L. plantarum significantly decreased the number of sulphite-reducing Clostridia spp. within a week of starting intake.

Treatment with B. infantis was shown to cause a significant reduction in a composite IBS score which included abdominal pain and bloating and difficulties with bowel movements. This was also associated with a change in PBMC cytokine production as assessed by the ratio of IL-10 to IL-12."


Lactobacillus reuteri accelerates gastric emptying and improves regurgitation in infants.
"In infants with functional GER, L. reuteri DSM 17938 reduce gastric distension and accelerate gastric emptying. In addition, this probiotic strain seems to diminish the frequency of regurgitation."

Effect of Bacillus subtilis PB6, a natural probiotic on colon mucosal inflammation and plasma cytokines levels inflammatory bowel disease.
"The pathophysiology of inflammatory bowel disease (IBD) involves the production of diverse lipid mediators, namely eicosanoid, lysophospholipids, and platelet-activating factor, in which phospholipase A2 (PLA2) is the key enzyme. Thus, it has been postulated that control of lipid mediators production by inhibition of PLA2 would be useful for the treatment of IBD. This hypothesis has been tested in the present study by examining the therapeutic effect of a novel natural probitic Bacillus subtilis PB6 (ATCC- PTA 6737). B. subtilis PB6 is found to secrete surfactins (cyclic lipopeptides) which have anti-bacterial potential. These surfactins inhibit PLA2, a rate-limiting enzyme involved in the arachidonic acid associated inflammatory pathway and could downregulate the inflammatory response by regulating the eicosanoid and cytokine pathways. With this concept, an experimental animal trial has been conducted in a rat model of 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. The oral administration of PB6 suppresses the colitis as measured by mortality rate, changes in the weight gain, colon morphology and the levels of plasma cytokines. The animals treated orally with PB6 at 1.5 x 10(8) CFU/kg thrice daily from day 4 to 10 significantly improve gross pathology of the colon and regain the colonweight to normal (p < 0.05), compared to TNBS-induced positive control. The plasma levels of pro-inflammatory cytokines (TNF-alpha, 1L-1beta, IL-6 and IFN-gamma) are also significantly lowered (p < 0.05) and anti-inflammatory cytokine (IL-I0 and TGF-beta) significantly (p < 0.05) increased after the oral administration of PB6 on day 11. The present study supports the concept that PB6 inhibits PLA2 by the secreting surfactins. In a clinical investigation, it is found to be well tolerated by all the healthy volunteers."

This is an article with more information about B.Subtilis and it's role in human health.  Sources of this probiotic include MegaSporeBiotic, PeakBiotic, and NST Probiotics.

Immune Modulation

"in the subset of forty-four randomized subjects providing biological samples, we showed that consumption of B. subtilis CU1 significantly increased fecal and salivary secretory IgA concentrations compared to the placebo. A post-hoc analysis on this subset showed a decreased frequency of respiratory infections in the probiotc group compared to the placebo group. Taken together, our study provides evidence that B. subtilis CU1 supplementation during the winter period may be a safe effective way to stimulate immune responses in elderly subjects."
Allergy and Mast Cell Response

Specific probiotics alleviate allergic rhinitis during the birch pollen season
"Birch pollen allergy was shown to be associated with changes in fecal microbiota composition. The specific combination of probiotics used (Lactobacillus acidophilus and Bifidobacterium lactis) was shown to prevent the pollen-induced infiltration of eosinophils into the nasal mucosa, and indicated a trend for reduced nasal symptoms."

"Human peripheral-blood-derived mast cells were stimulated with Lactobacillus rhamnosus (L. rhamnosus) GG (LGG(®)), L. rhamnosus Lc705 (Lc705), Propionibacterium freudenreichii ssp. shermanii JS (PJS) and Bifidobacterium animalis ssp. lactis Bb12 (Bb12) and their combination.

LGG and Lc705 were observed to suppress genes that encoded allergy-related high-affinity IgE receptor subunits α and γ (FCER1A and FCER1G, respectively) and histamine H4 receptor. LGG, Lc705 and the combination of four probiotics had the strongest effect on the expression of genes involved in mast cell immune system regulation, and on several genes that encoded proteins with a pro-inflammatory impact, such as interleukin (IL)-8 and tumour necrosis factor alpha. Also genes that encoded proteins with anti-inflammatory functions, such as IL-10, were upregulated.

CONCLUSION: Certain probiotic bacteria might diminish mast cell allergy-related activation by downregulation of the expression of high-affinity IgE and histamine receptor genes, and by inducing a pro-inflammatory response."


Immunomodulatory effects of potential probiotics in a mouse peanut sensitization model
"Prophylactic treatment with both HMI001 ( L. Salivarius) and LCS ( L. casei Shirota) attenuated the Th2 phenotype (reduced mast cell responses and ex vivo IL-4 and/or IL-5 production).  In contrast, WCFS1 ( L. Plantarum) augmented the Th2 phenotype (increased mast cell and antibody responses and ex vivo IL-4 production).  In vitro PBMC screening was useful in selecting strains with anti-inflammatory and Th1 skewing properties. In case of HMI001 (high IL-10/IL-12 ratio) and LCS (high interferon-γ and IL-12), partial protection was seen in a mouse peanut allergy model. Strikingly, certain strains may worsen the allergic reaction as shown in the case of WCFS1."

Effect of a New Synbiotic Mixture on Atopic Dermatitis in Children: a Randomized-Controlled Trial
"This study provides evidence that a mixture of seven strains of probiotics and Fructooligosaccharide can clinically improve the severity of AD in young children. Further studies are needed to investigate the effects on underlying immune responses and the potential long term benefits for patients with AD.

In a randomized, double-blind, placebo-controlled trial, we aimed on studying the clinical and immunologic effects of a mixture of seven strains of probiotic bacteria (Lactobacillus casei, Lactobacillus rhamnosus, Streptococcus thermophilus, Bifidobacterium breve, Lactobacillus acidophilus, Bifidobacterium infantis, Lactobacillus bulgaricus) and Fructooligosaccharide in the treatment of AD in infancy and early childhood."


Screening selected strains of probiotic lactic acid bacteria for their ability to produce biogenic amines (histamine and tyramine)
"The aim of this study was to investigate the production of biogenic amines (BA), histamine and tyramine by some probiotic lactic acid bacteria (LAB). Fifteen strains representing six LAB species were screened qualitatively by growing them in a decarboxylase medium. Lactobacillus casei (TISTR 389) and Lactobacillus delbrueckii subsp. bulgaricus (TISTR 895) were found to produce BA. The highest levels of histamine (1820.9 ± 3.5 mg L−1) and tyramine (5486.99 ± 47.6 mg L−1) formation were observed for the TISTR 389 strain, while TISTR 895 produced only histamine (459.1 ± 0.63 mg L−1) in the decarboxylase broth. Biogenic amine potential was not observed for the Lactobacillus acidophilus, Lactobacillus lactis subsp. lactis,Lactococcus lactis subsp. lactis, and Lactobacillus plantarum strains studied. This study confirmed that BA formation is strain dependent and not related to the species. "

"There is increasing, but largely indirect, evidence pointing to an effect of commensal gut microbiota on the central nervous system (CNS). However, it is unknown whether lactic acid bacteria such as Lactobacillus rhamnosus could have a direct effect on neurotransmitter receptors in the CNS in normal, healthy animals. GABA is the main CNS inhibitory neurotransmitter and is significantly involved in regulating many physiological and psychological processes. Alterations in central GABA receptor expression are implicated in the pathogenesis of anxiety and depression, which are highly comorbid with functional bowel disorders. In this work, we show that chronic treatment with L. rhamnosus (JB-1) induced region-dependent alterations in GABAB1b mRNA in the brain with increases in cortical regions (cingulate and prelimbic) and concomitant reductions in expression in the hippocampus, amygdala, and locus coeruleus, in comparison with control-fed mice. In addition, L. rhamnosus (JB-1) reduced GABAAα2 mRNA expression in the prefrontal cortex and amygdala, but increased GABAAα2 in the hippocampus. Importantly, L. rhamnosus (JB-1) reduced stress-induced corticosterone and anxiety- and depression-related behavior. Moreover, the neurochemical and behavioral effects were not found in vagotomized mice, identifying the vagus as a major modulatory constitutive communication pathway between the bacteria exposed to the gut and the brain. Together, these findings highlight the important role of bacteria in the bidirectional communication of the gut–brain axis and suggest that certain organisms may prove to be useful therapeutic adjuncts in stress-related disorders such as anxiety and depression."

'Psychobiotic' May Help Ease Stress, Improve Memory
"Taking a probiotic strain of Bifidobacterium longum reduced physiologic and psychological stress and led to a modest improvement in memory in a small pilot study of healthy men.

In response to acute stress, B longum NCIMB 41676 led to a reduction in cumulative output of the stress hormone cortisol, as well as a blunted increase in subjective anxiety. On the questionnaire, the men reported being less stressed and anxious while taking the probiotic. They also showed subtle improvement on a visual memory task after receiving the probiotic, as well as altered EEG output.

"This study represents a proof of principle," Dr Clarke said. "The question we are asking now is, can we advance this further and can we use these psychobiotics to deal with the stressors that we encounter on the roller coaster of life, or develop further psychobiotics for patients with stress-related disorders such as depression or anxiety."


Assessment of psychotropic-like properties of a probiotic formulation (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) in rats and human subjects.
"In a previous clinical study, a probiotic formulation (PF) consisting of Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 (PF) decreased stress-induced gastrointestinal discomfort. Emerging evidence of a role for gut microbiota on central nervous system functions therefore suggests that oral intake of probiotics may have beneficial consequences on mood and psychological distress. The aim of the present study was to investigate the anxiolytic-like activity of PF in rats, and its possible effects on anxiety, depression, stress and coping strategies in healthy human volunteers... Daily subchronic administration of PF significantly reduced anxiety-like behaviour in rats (P < 0·05) and alleviated psychological distress in volunteers, as measured particularly by the HSCL-90 scale (global severity index, P < 0·05; somatisation, P < 0·05; depression, P < 0·05; and anger-hostility, P < 0·05), the HADS (HADS global score, P < 0·05; and HADS-anxiety, P < 0·06), and by the CCL (problem solving, P < 0·05) and the UFC level (P < 0·05). L. helveticus R0052 and B. longum R0175 taken in combination display anxiolytic-like activity in rats and beneficial psychological effects in healthy human volunteers."

Thursday, November 19, 2015

The Microbiome

There are about 10 times more microbial cells in and on our bodies than there are human cells.  These microbes are referred to as the microbiome, which is divided loosely into separate biomes based on location (such as the gut microbiome, the sinus microbiome, etc).  The way that these microbes affect and influence the health and functioning of our bodies has not been understood much in the past, but is increasingly being studied now.  The microbes that live in and on us play many roles, including aiding in digestion, providing certain enzymes and nutrients, regulating out immune system and inflammation, keeping pathological microbes in check, and even regulating the expression of some of our genes. New evidence shows that micro organisms are even the source of some of our genes which have been acquired through a process called horizontal transfer.

There are many factors that influence the health and diversity of our microbiome.  Many medications alter our flora, especially antibiotics, but many others do too such as oral contraception.  What we eat, what personal care products we use, and what we use to clean our homes are also major factors.  Antibiotics can have a devastating effect on the microbiome, something which is only now being appreciated, and which may explain many of the side effects and unintended outcomes of widespread antibiotic use.  A recent article about research being done on the role of the microbiome in autism and other health conditions called Autism's bacteria link gains credence provides a basic introduction to these factors:

"But changes in the past century have altered the microbial balance as societies relied too heavily on antibiotics, disinfectants, C-section deliveries and a diet of refined carbohydrates. Those changes replace inner gardens of helpful bacteria with a harmful mix that makes compounds that in excess can damage the digestive system, brain, immune system, and the way cells metabolize energy.  The damage is likely worse in babies whose brains and immune systems are developing, MacFabe says. But the damage also occurs throughout life."

The Origins of the Microbiome

A fetus growing in it's mother's uterus is sterile until birth, when it is colonized by bacteria.  In a vaginal birth, the baby is colonized by the mother's vaginal and fecal flora.  Babies born by c-section are instead colonized by the bacteria present in the room during birth.  Touching and kissing the baby is another source of flora.  To learn more about this read The infant gut microbiome: New studies on its origins and how it's knocked out of balance.  Once the baby is colonized at birth, the gut flora is further influenced by whether the baby is breastfed or formula fed and when solid food is started and what foods are eaten.

Maternal prenatal stress is associated with the infant intestinal microbiota.
Psychoneuroendocrinology. 2015 Mar;53:233-45
"Results showed that maternal prenatal stress, i.e., either reported stress or elevated basal maternal salivary cortisol concentrations or both, was strongly and persistently associated with the infants' microbiota composition as determined by a phylogenetic microarray. Infants of mothers with high cumulative stress (i.e., high reported stress and high cortisol concentrations) during pregnancy had significantly higher relative abundances of Proteobacterial groups known to contain pathogens (related to Escherichia, Serratia, and Enterobacter), and lower relative abundances of lactic acid bacteria (i.e., Lactobacillus, Lactoccus, Aerococcus) and Bifidobacteria, altogether characteristics of a potentially increased level of inflammation. Furthermore, this aberrant colonization pattern was related to more maternally reported infant gastrointestinal symptoms and allergic reactions. In conclusion, clear links were found between maternal prenatal stress and the infant intestinal microbiota and health. Although causality cannot be concluded, the results suggest a possible mechanism by which maternal prenatal stress influences the offspring development. These results suggest a potential for bacterial interventions to enhance offspring health and development in pregnant women with stress."

How Diet Affects the Microbiome

What an individual eats has a profound impact on the population and diversity of their gut microbiota.  It is also true that there are differences between normal gut flora in groups of people living in vastly different parts of the world and eating vastly different diets.  A study was done comparing the gut flora of children in Europe with that of children in a rural village in Burkina Faso in west Africa that showed how significant these difference can be and suggests that our gut flora have evolved along with us to reflect what we eat.

Study links common food additives to Crohn's disease, colitis
The study being reported on here looked at two emulsifiers commonly used in processed food and their effect on gut health and gut flora, polysorbate 80 and carboxymethylcellulose.

"A key feature of inflammatory bowel diseases and metabolic syndrome is a change in the gut microbiota - the roughly 100 trillion bacteria that inhabit the intestinal tract - in ways that promote inflammation. In mice given emulsifiers, the bacteria were more apt to digest and infiltrate the dense mucus layer that lines and protects the intestines."

The Microbiome in Health and Disease

In this study Foxp3 T Cells Regulate Immunoglobulin A Selection and Facilitate Diversification of Bacterial Species Responsible for Immune Homeostasis (you can read about what this study means here) it is found that:

"They discovered that the immune system "sees" and responds differently to different bacterial communities. Rich and balanced bacterial communities seem to be perceived as "self" and induce a quick maturation of the immune system and gut responses (induction of regulatory T cells and IgA), while a poor and unbalanced bacterial community is apparently perceived as "non-self" and induces responses aimed at eliminating it (T cells with inflammatory properties and IgG or IgE responses)."

Understanding an individual's microbiome is part of the emerging paradigm shift going on in medicine right now to individualized medicine, which is an approach to understanding and treating disease based on an individual's genetics, microbiome, environmental factors, and any other factors that influence the health of an individual.  In this new paradigm, rather than classifying patients together by diagnosis and then treating each of them with the same methods it is a way to individualize treatment to the individual's specific needs.  This brief interview from a medical conference held in 2015 on the cutting edge research in digestive disease gives a little more detail on how this paradigm shift relates to the gut and it's microbiome.

Restoring Microbial Balance Key to Keeping Sinuses Healthy
"A new study by Dr. Goldberg and colleagues likewise concludes that the health of our sinus cavities, once thought to be largely sterile, may be highly dependent on the composition of their microbial residents...Beyond a significant decrease in the diversity of microorganisms among the patients, the researchers found a noticeable drop in a group of bacteria known as Lactobacilli, long associated with maintaining health in the gut. Concurrently, the researchers saw an increase in a little-known potential pathogen called Corynebacterium tuberculostearicum..."Central to the concept that we’re putting forward is that there is a protective mechanism in a normal sinus that comes about as a result of the microbiome,” Dr. Goldberg said."

The dormant blood microbiome in chronic, inflammatory diseases
"A number of recent, sequence-based and ultramicroscopic studies have uncovered an authentic blood microbiome in a number of non-communicable diseases. The chief origin of these microbes is the gut microbiome (especially when it shifts composition to a pathogenic state, known as 'dysbiosis'). Another source is microbes translocated from the oral cavity. 'Dysbiosis' is also used to describe translocation of cells into blood or other tissues. To avoid ambiguity, we here use the term 'atopobiosis' for microbes that appear in places other than their normal location. Atopobiosis may contribute to the dynamics of a variety of inflammatory diseases. Overall, it seems that many more chronic, non-communicable, inflammatory diseases may have a microbial component than are presently considered, and may be treatable using bactericidal antibiotics or vaccines."

Gut dysbiosis and detection of "live gut bacteria" in blood of Japanese patients with type 2 diabetes
"Mounting evidence indicates that the gut microbiota are an important modifier of obesity and diabetes...The counts of the Clostridium coccoides group, Atopobium cluster, and Prevotella (obligate anaerobes) were significantly lower, while the counts of total Lactobacillus (facultative anaerobes) were significantly higher in fecal samples of diabetic patients than in those of control subjects. Especially, the counts of Lactobacillus reuteri and Lactobacillus plantarum subgroups were significantly higher. Gut bacteria were detected in blood at a significantly higher rate in diabetic patients than in control subjects (28% vs. 4%, P < 0.01), and most of these bacteria were Gram-positive...The high rate of gut bacteria in the circulation suggests translocation of bacteria from the gut to the bloodstream."

The Treatment-Naive Microbiome in New-Onset Crohn’s Disease
"Inflammatory bowel diseases (IBDs), including Crohn’s disease (CD), are genetically linked to host pathways that implicate an underlying role for aberrant immune responses to intestinal microbiota. However, patterns of gut microbiome dysbiosis in IBD patients are inconsistent among published studies. Using samples from multiple gastrointestinal locations collected prior to treatment in new-onset cases, we studied the microbiome in the largest pediatric CD cohort to date. An axis defined by an increased abundance in bacteria which include Enterobacteriaceae, Pasteurellacaea, Veillonellaceae, and Fusobacteriaceae, and decreased abundance in Erysipelotrichales, Bacteroidales, and Clostridiales, correlates strongly with disease status. Microbiome comparison between CD patients with and without antibiotic exposure indicates that antibiotic use amplifies the microbial dysbiosis associated with CD. Comparing the microbial signatures between the ileum, the rectum, and fecal samples indicates that at this early stage of disease, assessing the rectal mucosal-associated microbiome offers unique potential for convenient and early diagnosis of CD."
It has recently been discovered that certain parasites are able to modulate the immune system of the host by communicating with the host's microbiome.  Some of these parasites are being used therapeutically to treat inflammatory and allergic disorders, although it was not fully understood why the treatment was effective.  Here findings are discussed that show that the parasites are inducing the microbes of the gut to produce certain short-chain fatty acids that modulate the immune system.

In addition, a compromised immune system can alter the microbiome of the gut, leading to intestinal disease such as Inflammatory Bowel Disease.

Study Finds Gut Bacteria Help Prevent Post Traumatic Stress Disorder (PTSD)

Monday, November 24, 2014

Treating Yeast

Perhaps one of the most common pathogens to cause infections in people with autism, ME/CFS, and a number of other health challenges is yeast, often called Candida (which is one kind).  Yeast cells live in all of our bodies as part of our microbiome, and are usually kept in check by the balance of microbes and by our immune system.  However, when the gut biome becomes disturbed, or our immune system becomes unable to fight adequately, yeast can grow out of proportion and lead to an opportunistic infection.  Many mainstream doctors will say that it is pointless to test for yeast because everyone has it, but they are missing the point that testing can be much more sensitive and accurate than a simple "yes/no".

There are so many symptoms of yeast that it is hard to list them all, and can make identifying a yeast infection by symptom challenging, since there can be so many potential causes of these symptoms.  However, some symptoms are more common than others, and taken together with risk factors looking at a person's symptoms is often the first step.  Yeast can be local or systemic.  Local symptoms may be a rash on the skin, usually in a skin fold or somewhere moist.  Vaginal yeast infections are common and cause itching and burning.  Yeast in the GI tract may appear as white, stringy threads in the feces that look like melted cheese.  You may also see small white balls or patches on and around the anus and in the feces, as well as a bright red ring around the anus and redness between the butt cheeks.

Signs of systemic infection include emotional reactivity such as rages and crying fits, episodes of laughter that seem out of the blue, difficulty sleeping, night terrors, spaciness, rigidity, limiting of food choices, GI distress, urinary leaking or accidents (including bed wetting), sensory sensitivities (especially sensory avoidance), headaches, sore throat, sinus infections, congestion, mucousy stools, teeth grinding, constipation, nausea, vomiting, sinus infections, bad breath, rough skin or "sandpapery" rash, peeling skin (especially around fingernails and on feet), craving sugars and simple carbs, gas, and bloating, among many others.

Options for treatments for yeast:

A note about yeast "die-off" (also called a healing reaction or Herxheimer reaction)- when a person begins to kill yeast, they often experience unpleasant symptoms and feel worse at first.  This is because the dying yeast is taxing the person's detoxification systems, which have already been taxed by the presence of the yeast.  The degree to which a person experiences this depends on a number of factors, including how much yeast they had in their system to begin with, how quickly the yeast is dying, and how robust their detoxification systems are naturally.  Epsom salt baths can ease the discomfort of die-off by supporting detox.  Activated charcoal can be taken 30 to 60 min after taking an anti-fungal treatment to "mop up" the toxins from the dying yeast in the gut, sparing the body from having to process it.  Because die-off can be stressful to the body, many people choose to ease into yeast killing slowly enough to keep the symptoms of die-off mild and manageable.  This can mean starting with low doses of anti-fungal treatments or making dietary changes slowly over a period of time.

Diet- modifying the diet is usually the first-line defense in addressing yeast.  In simple terms, this means removing sugar and simple starches from the diet.  There are about a million versions of the anti-yeast diet, which you can easily find via a google search.  Many have their advantages and reasons for eliminating certain foods.  Be aware that many of these diets have been "watered down" to make them more appealing to people and easier to do, but at the expense of effectiveness.  Any diet that includes sugars or starches such as sweet potato, rice, or corn will not be very effective.  There is a lot of disagreement about whether honey is a problem or not and this seems to be very individual.  Honey is itself anti-fungal, meaning it kills yeast.  Most honey from supermarkets in the US is altered, however, and can be diluted with other sugars, including HFCS.  So you will need to figure out for yourself if honey works for you.  Yeast will happily feed on what is difficult for our own bodies to digest, which means that many complex carbs such as beans and grains can be major yeast feeders.  The stricter and more effective anti-yeast diets eliminate many if not all of these foods.

Another area of disagreement is about fermented foods.  For some people these can be very beneficial in fighting yeast, as they provide probiotics, as well as other factors that support gut and immune function.  They also contain metabolites of bacteria and yeast, depending on the type, which can be too much for a system already burdened with internally-produced metabolites, so may exacerbate symptoms.  These foods can also be a problem for people with histamine sensitivity.  Many people who address yeast through diet find that they also need to avoid high mold foods, which include tomato, berries, dried fruits, nuts, mushrooms, and ferments including vinegar.  Tolerance of fruit in a yeast fighting diet also varies from person to person.  In general, a more paleo-type diet is best.  If you are very serious about fighting yeast, the best two diets are the Specific Carbohydrate Diet and the GAPS Diet.  The Body Ecology Diet (BED) is also popular and an option for people who need or want to eat fewer animal foods, but is less based on science.

Enzymes- There are several enzymes available that break down the yeast wall and kill it.  These are easy to use and can be very effective, if taken on an empty stomach (if taken with food they will simply digest the food instead).  These include Candex, Candidase, and No-Fenol.  No-Fenol was actually developed to aid in the tolerance of foods high in phenols, but it contains an enzyme that does this by breaking down plant cell walls and many users found that if taken on an empty stomach it seems to have similar action as Candex and Candidase.  From the manufacturer's site "xylanase is the major component of No-Fenol, and is an enzyme used to breakdown the structural components of plant cell walls, which are primarily very complex carbohydrates."  (Note about Candex and Candidase- Candidase includes a protease enzyme as well, which helps break down the "innards" of the yeast cell after it dies.  Some people find this helpful in reducing the symptoms of die-off while others don't, like many things involving yeast, this seems to be very individual).

Probiotics- yeast exists in our bodies as part of complex ecosystems and can cause problems when those systems become disrupted or altered.  Probiotics help to restore the systems so that the yeast can be kept in check naturally by the body again.  Probiotics can also be very effective in the short term to kill yeast by out-competing it.  For this reason they should be started at low doses and worked up slowly.  For yeast in the sinuses, a probiotic capsule can be opened and put directly in the mouth or gargled before bed.  There is as much disagreement about which probiotics are best, and how best to use them, as there is about dietary options.  Many people find that products that include prebiotics such as inulin- which are meant as "food" for the probiotics- can cause problems.  Some popular and effective probiotics include: VSL #3BioGaiaBioKultsaccharomyces boulardii (often used in conjunction with other probiotics), Florastor is a popular brand of s. boulardii, Custom Probiotics (which are apparently grown on corn), TherelacThreeLac and FiveLac, Primal Defense (which is made of soil-based organisms), and ProBio by Enzymedica.  Probiotics products often contain allergens such as dairy and corn so always be cautious.  Also, some people react to strep strains, such as s. thermophilius (which is found in yogurt), and which are commonly found in probiotic supplements (they are usually beneficial but can trigger PANDAS in some people).

Medications- the primary two pharmacological meds used to kill yeast are Nystatin and Diflucan.  The primary difference between the two is that Diflucan is systemic, while Nystatin stays in the gut and acts locally.  Because Diflucan is absorbed into the bloodstream and acts systemically, there is a concern that it may negatively affect the liver if taken for long periods of time.  These meds are generally used for at least 3 months at a time in order to assure that enough yeast is killed to keep it from coming right back once the med is stopped.

Herbs and Supplements: there are many, many substances taken to kill yeast.  Some of the most common and effective ones include raw garlic, coconut oil, berberine (also called Oregon Grape Extract), uva ursi, GSE (grapefruit seed extract), caprylic acid (derived from coconut oil), biotin (a B vitamin that keeps yeast from changing into it's more pathogenic forms), CytoFlora, oil of oregano, olive leaf extract, tea tree oil, manuka honey, calendula, gentian violet (often used for oral thrush in nursing mothers and babies), goldenseal, pau d'arco, and turmeric.

More on the microbiome:

This piece from NPR gives a good overview of the origins and importance of the microbiome in our health, as well as some of the factors that can disrupt it.

A new study shows that there have been major changes in the human microbiome in very recent times.

More on yeast:

Hyperactivity, ADHD and the Yeast Connection

Sunday, November 9, 2014

Identifying and Treating H. Pylori Infection

These are notes from an interview about H. Pylori with Dr Daniel Kalish, DC :

H. Pylori is a bacterial infection that can be caught form another person, and can also be contracted by eating under-cooked food.  It results in an infection of the stomach that compromises the functioning of the stomach, which can lead to damage to the cells that line the stomach (parietal cells), which in turn can cause poor production of hydrochloric acid.  This means that the food in the stomach isn't properly broken down, which compromises digestion.  The food gets passed along into the small intestines and just sits there, since it hasn't been broken down, and can feed bacteria and yeast, leading to gas and bloating.  This also leads to inadequate absorption of nutrients from the food, since it isn't being broken down properly.  Bad breath can also be a sign.

H. Pylori can also cause heartburn, which occurs when the valve at the top of the stomach that is supposed to keep the acid in the stomach becomes weak and allows the acid to go up into the esophagus.  When the food passes out of the stomach and into the small intestine, it is supposed to be a certain acidity, which is what triggers the pancreas to excrete enzymes and the gallbladder to release bile.  This also can lead to poor digestion, gut infections, and poor nutrient absorption.  Acid blocking drugs actually allow the infection to get worse rather than addressing the problem.

Many people do not have specific gut symptoms from chronic infections such as H. Pylori, but they do have more global symptoms such as fatigue.  There is also a chronic inflammation situation going on in the body, which can manifest as depression, etc.  H. Pylori can be passed through kissing, sharing food, sexual contact, and more.  It seems that some people can carry it and have no symptoms, and some people believe that at least certain strains can be healthy to have.  The problem seems to be when the infected person is stressed or their immune system is otherwise weakened.

Testing was originally looking for antibodies, which may not indicate a current infection.  Also, in a full blown infection antibody levels can drop, while the infection is still there.  There is also a breath test which can work if you have a new, severe infection.  It can also be looked for in an endoscopic exam, which also misses it frequently and is invasive.  None of the standard tests are very reliable.  Another option is the antigen test. An antigen is the thing that an antibody is reacting to, it is a part of the pathogen itself.  If this test is positive, then the infection is current and active.  It's done from a stool sample.  It's not yet done in conventional medicine.  It can still be a false negative, since the pathogen may not have come out in that particular sample.

For decades, doctors thought that stress caused ulcers, which was because stress brings down the immune system which then allows the H. Pylori infection to ramp up.  One doctor who suspected H.Pylori as the causal agent in ulcers actually gave himself the infection to prove his point.  He had endoscopic pictures taken of his healthy stomach beforehand, gave himself H. Pylori, developed  a bleeding ulcer, had it documented, took antibiotics, and documented that the ulcer was cured this way.  This work led to a nobel prize.  Conventional medicine is so focused on acute, serious infections, and has tended to ignore the impact of chronic infections.

Consequences for not treating the infection can be severe, including stomach and intestinal cancer.  When this infection is treated it can make a huge difference in people's lives.  Conventional doctors often don't want to treat this infection unless there are signs of major tissue injury, such as a bleeding ulcer, because standard treatment is 2 weeks of a very strong antibiotic.  There are other treatment options however.

Having a chronic infection in the stomach, that is inflammatory, leads to increased cortisol production (cortisol helps control chronic inflammation) which places stress on the adrenals.  Also, if there are other sources of stress in the body, physical or emotional, this can tax the adrenals, use up cortisol, and make it harder for the adrenals to control the inflammation in the stomach.  This is how stress can lead to the infection flaring up.  The adrenals also control the production of something called secretory IgA ( also called SIgA), which are immune factors that line the mucosal tissues of the body, such as the GI tract.  When we're stressed, SIgA levels drop, and this can allow infections to take hold or flare up (this includes in the respiratory tract, the sinuses, the GI tract, in the genitourinary tract, and on the skin).

Dr Kalish was trained to focus on treating the adrenals first, rather than focusing on eliminating the infection first.  This can begin with dealing with emotional stress, making sure to eat good food, sleep well, and get basic exercise.  He also uses adrenal protocols to get the adrenals working well for 60 days before going after the bugs.  In deciding when to use the antibiotics treatment, or when to use the more natural herbal approach, he says this is an individual decision and not the same for all patients.  One factor is if you have an ulcer..in which case you may want to go ahead and use the antibiotics, and not wait around for the herbals to work. It is worth noting though that the antibiotics used here are strong and can have negative side effects, and the herbal treatment is very successful and safe.  He suggests using Mastica gum, to fight the infection, but warns that this infection is a "host specific problem" and that the gum is not likely to work unless the person strengthens their immune system.  In addition to the Mastica gum, he will also usually include antibacterial herbs such as Oil of Oregano or Olive Leaf Extract.  He also includes a powerful anti-inflammatory agent such as DGL, a product of licorice.  This protocol takes about 2 months, in addition to the 2 months of prep of working on the adrenal glands first.  It is worth considering testing family members and partners to prevent the person from being reinfected.  In a very young child or infant, what you might see is the child refusing many foods or developing strong preferences and avoidance of foods.


Monday, September 9, 2013

Gut Health Interview with SCDLifestyle

These notes are for a podcast from Underground Wellness (click here to listen) featuring Jordan Reasoner and Steve Wright of the website SCDLifestyle,com  http://scdlifestyle.com/

The show is about gut and digestive health but largely focused on what our bowel movements tell us about these two areas of our health.  Basically, our poop is an "output variable" that gives us information about what is going on inside our systems.  Healthy elimination of stool occurs usually between 1 and 3 times per day, and should involve no straining or discomfort.  They recommend consulting the Bristol Stool Scale for more information about what our poop tells us and what is healthy. 

What are factors that cause less than ideal poop?

First factor is eating a real food diet, such as paleo, WAPF, primal.  Eating the standard American diet is problematic and should be addressed first.  If you are eating real food and still have poop issues, you are most likely dealing with chronic illness.  There are three main body systems involved in producing healthy poop, and they tend to find that at least 1 or 2 of them are diseased in clients with poop problems.  These include the hormonal axis (the HPA axis), which is how the brain and the body communicate, which can include sex hormones, thyroid hormones, and stress hormones like cortisol.  The GI tract is another relevant system, which seems obvious but can be involved in more complex ways than people sometimes think, including issues like SIBO, leaky gut, parasite and bacterial infections, intestinal inflammation.  The third main system is the liver detox system which includes the liver as well as the other ways that the body removes toxins, including the the lymph system, the circulatory system,  and the skin.

More on the hormonal axis....

For many people there is a stressful triggering event that leads to a downturn in people's GI health, such as a trauma, a death, an accident, etc.  This can lead to itchy eyes, acne, poor libido, which indicate the hormonal axis coming apart.  Cortisol, produced by the adrenal glands in response to stress, is the primary anti-inflammatory hormone in the gut, and when people aren't able to produce enough inflammation in the gut gets out of control.  With ongoing stress the communication pathways between the brain and the adrenals get worn out.  Then we can't shut off the inflammation in the gut.  Pretty much everyone with any gut issues and/or food intolerances has leaky gut to some degree.  Proper cortisol levels are what seals up the leaky gut. 

DHEA is also made by the adrenal glands and is very correlated with the immune system in the gut.  As the hormone system in the gut breaks down, we also lose our immune function in the gut.  Adrenal fatigue causes us to lose our secretory IgA function in the gut.  This is what is primarily responsible for taking care of yeast, bacteria, parasites, and even food particles that didn't get broken down int the gut.  This can also cause new food sensitivities to occur. 

What are the specific issues in the gut to look for?

Inflammation and leaky gut are a vicious cycle.  The majority of their clients test positive for parasitic and bacterial infections in the large intestine such as H. Pylori, and issues like SIBO in the small intestine.  SIBO also tends to come from inability to digest complex carbohydrates. 

What about liver detoxification pathways?

Leaky gut allows toxins like LPS (which come from the infections in the gut) into the body, foods that aren't being broken down enough.  The liver has to work to process medications and supplements that we take to address our gut issues.  Heavy metals and other environmental toxins also take out this system.  People with sluggish and overburdened livers are often the people who seem very sensitive to supplements, who can only take one brand, and who seem to do poorly on prescribed protocols needing to go slowly.  The liver is a big part of regulating hormones, so you can't hope to balance hormones without addressing the liver.  Skin issues often indicate an overflow of toxins from the liver that the body is excreting another way.  Constipation allows the body to reabsorb toxins that it's trying to excrete, which further burdens the liver.  This is called low grade endotoxemia.  (There is another interview on UW with Tom O'Bryan about LPS toxicity).

Examples from clients 

They say that about half of their clients have had issues relating to dysfunction in these 3 systems from birth, and about half of the clients had a triggering stressful incident that followed very good health, which led to disease onset.  Problems can include constipation issues from childhood, headaches, chronic sinus infections, menstrual problems from the onset of menstruation, etc. 

Misc from questions...

Are routine colonoscopies necessary?  They point out that many problems can occur from the prep process for the scopes, which can clean out the good bacteria from your gut so probiotics are really important to follow up with.  What causes pencil thin poops?  This can be caused by blockages, make sure to avoid grains, than do stool testing.  They suggest 2 tests, a BioHealth 401H (which is a stool culture) and MetaMetrix 2105.  It's important to make sure that there isn't a bacterial or parasitic infection in the gut.  Especially if the person is eating areal food diet, look for a parasitic or bacterial infection right away.

Some supplements speed up the bowels, such as protein powders (like whey and casein), also caffeine can speed along bowel movements.  

NAC is good for boosting glutathione status to support the liver.


Not eating enough fat can cause constipation, because fat content can trigger peristalsis. 

Digestive enzymes are a very important to support digestion, especially if the gallbladder has been removed.  Loose stools or nausea indicate the need for more enzymes or other digestive support.

Functional medical practitioners use different labs and different tests than standard general practitioners do, which are much more advanced and turn up issues that general doctors and tests miss.  The page 6 gut infection case studies gives more info on the tests that these practitioners use.


Thursday, December 6, 2012

GAPS Diet Success Stories

I love success stories.  From the beginning they have given me hope and kept me going.  They have inspired me.  Most of all, as they say in Al Anon, "stick with the winners".  Those who have accomplished what I wish to accomplish have much to teach me.  When it comes to the GAPS diet (Gut and Psychology Syndrome) there are many success stories, some so amazing they'd be hard to believe if we hadn't also had such incredible results ourselves!

Many of these success stories I've heard directly from the family, or I've seen on various lists and yahoo groups, but here are a few that I've come across online:

Hannah's Story: 2 Years on the GAPS Diet Reverses Autism

This is the story of a child with verbal apraxia beginning to speak on the GAPS diet

This GAPS recovery story is from a woman who had serious mental health issues as well as physical issues (such as exhaustion, migraines, and chronic pain).

Kate's story (she suffered from depression, anxiety, and many chronic health conditions)

Scarlet's progress on the Paleo diet

A letter to Dr Natasha


I will be adding more, and feel free to share stories or suggest links in the comments section!

Tuesday, August 28, 2012

Critique of the NY Times Article "An Immune Disorder at the Root of Autism"

The article can be read here.  This article has a lot of truth in it, and is being widely circulated right now (at least on Facebook) and I wanted to say a few things about it.  The central role of immune dysregulation and inflammation in autism is something that is well supported by evidence.  This is not really something "new", so much as there has been a lessening of the unwillingness to consider biological aspects of autism recently.  Parents, doctors and medical researchers who have been studying the biology of autism and how to heal it have been aware of this for quite a while, and as the article states the health of the mother does seem to be very relevant for the child's risk of autism.  Again, not news if you actually follow this. I am VERY excited to see this information in the NY Times and I think it is a big step forward.  However, I would like to clarify some of the details in the article.

The author, while getting the gist right, clearly does not have the basic knowledge of the question of autism causality, the theories, and the evidence, to put this information in context and therefore to understand the implications.  For example the author says that popular awareness is fixated on vaccines as the cause of autism.  Well, anyone who has ever tried to speak about the reality of vaccine injury can attest that this is a fiercely denied idea by the majority of the public.  The second major error in the introductory paragraph is that the author claims that people are "fixated" on vaccines DESPITE recent developments in the scientific understanding of autism, when in reality these developments are what support the view of autism as vaccine injury in many cases.  This evidence explains the "how " and "why" of vaccine-induced autism.  Almost no journalists follow this science though, so they are not aware of this. 

This article makes another very common mistake that we see consistently in reporting on autism.  The author says that the reason put forth here for the cause of autism accounts for maybe one-third of cases, and then begins to speak about the theory as if it is the ONLY cause.  That is a very common mistake.  By the authors admission, two-thirds of cases of autism do not fit this explanation, or at least the way the author is understanding it.  Another common mistake is writing off as much as half of the increase in autism as better diagnosing or changes in diagnostic criteria.  While this may of course be an issue, it is a red herring and the frequency with which it is brought up undermines the urgency of the autism epidemic and undermines the credibility of autism families.  Ultimately it just keeps us focused on autism as a failure of parents, most often mothers, for either seeking a diagnosis for "free services" or out of ignorance that "kids are like that" or because expectations are too high about children's accomplishments. 

Also, because the author does not understand why some people draw a connection between autism and vaccinations, he does not understand that everything he puts forth here- about the role of infections and immune dysregulation- implicates vaccines.  Vaccines work (to the extent that they do) by simulating an infection and causing inflammation.  They are designed to make the immune system "think" that there has been a full-blown infection (despite the small amount of antigen delivered) by sending the message (chemically) for the immune system to over-react to the antigen.  This is the job of the adjuvant in the vaccine, and you can go to this post to see a presentation about the ways in which adjuvants have been shown to lead to auto-immunity, which is both defined by a dysregulated immune system and is widespread among people with autism and their families. 

The biomedical approach, which is the approach to treating autism rooted in biology and physiological and chemical causality for the symptoms of autism, is not just about vaccines.  In the model of biomed (and here), vaccines are one potential source of both toxicity and immune dysregulation, but they are not the only source for these things.  This is also true of mercury toxicity.  It is an issue relevant to vaccines, but vaccines have concerns beyond mercury and mercury can come from many sources other than vaccines.  In my family's case, the mercury came from my amalgam fillings.  This is one condition that fits this article well.  My fillings poisoned me, causing immune dysregulation and an auto-immune disorder in me, and then as my kids grew inside my body they were affected by the mercury and were born already poisoned. 

This article also rightly highlights the role of the microbial ecosystem that is part of our bodies.  Proper balance in this ecosystem is essential for health and disruptions in this system can be disastrous.  Dysbiosis (often in the gut, but not only there) is indeed one of the central biological features of autism.  However, the "hygiene hypothesis" tends to greatly oversimplify what is going on here.  It is not that some people lack microbes or were not exposed to enough of them, it's more a question that the transmission of our flora is being interrupted and changed so that children are not starting out with a robust enough system to function adequately.  Our flora is transmitted to us during birth from our mothers as we pass through the birth canal, and is then shored up by breastfeeding.  Birth interventions and lack of breastfeeding are so widespread that almost no one has not been affected, at least here in the US.  If your child, yourself, or any of the women who came before you ever took antibiotics, birth control pills, steroid medications, had any birth interventions, or were given formula (even if they were also breastfed) then your child has altered flora. 

What the "hygiene hypothesis" fails to account for is that not all microbes are interchangeable.  People with autism have no dearth of microbes and parasites in their bodies.  Parasite treatments are some of the most effective biomedical treatments around.  Likewise, people with autism have a heavy load of pathogenic microbes that are the cause of many of the symptoms.  This is the direct result of the immune dysregulation that this article discusses.  The problem is WHICH ONES they have and the difficulty their immune systems have in maintaining order in this system.  Interventions that restore balance in the flora by reducing pathogenic flora while re-introducing "friendly" flora have been very helpful in treating autism. 

I have no idea why he makes the claim that scientists studying the link between autism and inflammation are unaware of the role of our microbial ecosystems, or of an uneven distribution of autism around the world.  I've been following this research for years and this seems to be well established and understood.  Again, all I can guess is that this author, like nearly all reporters who write about autism, does not have the depth of knowledge of the research to be able to make reliable observations about it.  Also, within the autism community we are well aware of how autism is a disorder of modern living rather than something that is somehow missed in developing countries.  Many families immigrate to the US, only to have one or more children regress into autism, and then are unable to explain what autism is to relatives back in the home country who have simply never seen anything like it.  See my post on the high prevalence of autism among Somali immigrants in Minnesota for more about this.

Most of all, what the author is doing is missing the forest for the trees. Being born to a mother with asthma, or rheumatoid arthritis, or celiac disease, or metabolic syndrome, (or experiencing vaccine injury for that matter), are not "different paths" to autism.  They are all variations on the same theme.  In similar fashion, he states at the end that preventative medicine in the future will need to emulate the way humans lived in the past.  I couldn't agree more, and this is again a central idea for many people working to heal autism.  The modern diet bears almost no resemblance to the food that humans evolved eating.  In particular, humans did not evolve eating grains, and the milk supply that we have now has been altered by a recent genetic mutation and is not comparable to milk that we would have had access to even not long ago in the past.  Our environment has been saturated with chemicals that are known to be toxic and even to alter how our immune systems function.  Lastly, conventional medicine in the developed world has resulted in dramatic changes to our microbial ecosystem and relies heavily on the use of pharmacological medications, most of which strain the body in the same ways that we see in autism.   This article is a good first step but there is so much more to understand and do in regards to autism (and the other inflammatory disorders mentioned, which are indeed highly related) than giving everyone worms.


Sunday, April 8, 2012

New Discoveries Highlight How Little is Known of the Immune System

Much of what is called modern medicine is meant to interact with our immune system, and yet we know so little about how it works.  Antibiotics and vaccines have both been the mainstay of this, and while both have undoubtedly saved many lives (especially antibiotics), they have had unforeseen consequences.  Antibiotics alter the flora in our bodies, which account for 90% of the cells that make up our bodies, which can have profound implications for our long-term immune functioning. 

A new study, just published last month called Microbial Exposure During Early Life Has Persistent Effects on Natural Killer T Cell Function, shows how significant our early gut flora can be for our long-term immune function.  Antibiotics have become widely used during labor and the neonatal period.  No doubt this is necessary sometimes, but little concern is given for the possible long-term effects of this use and for the importance of taking protective measures.

"Colonization of neonatal—but not adult—GF (germ-free) mice with a conventional microbiota protected the animals from mucosal iNKT accumulation and related pathology. These results indicate that age-sensitive contact with commensal microbes is critical for establishing mucosal iNKT cell tolerance to later environmental exposures." 

Another study, also just published, challenges a long held belief that antibodies are both necessary and the most significant factor in immunity against viruses.  One of the cornerstones of the use of vaccines is that antibody levels (titers) are assumed to be both necessary for immunity and the most accurate measure of immune status.  From an article about the study in Science News:


"A new study turns the well established theory that antibodies are required for antiviral immunity upside down and reveals that an unexpected partnership between the specific and non-specific divisions of the immune system is critical for fighting some types of viral infections."

Saturday, February 18, 2012

Autism and the Gut Microbiome

I have written a more general post about the connection between autism and problems in the gut, but want to focus specifically on the imbalanced microflora that is such a major part of this.  Many of the symptoms of autism can result directly from the toxins and metabolites produced by the overgrowth of pathogens, and other symptoms can result indirectly from these imbalances.  These symptoms can include sensory issues such as sensitivity to light and sound, obsessive compulsive disorder or tendencies, stimming, self-injurious behavior, aggression, sleep problems, pickiness and food aversions, hyperactivity, anger and rage, other mood issues, rigidity, speech problems, difficulty with processing language, allergies, altered sensitivity to pain, and many more.  These imbalances can lead to or worsen common biological conditions in autism such as mitochondrial dysfunction, high histamine levels, high oxalate levels, leaky gut and IgG food allergies, and possibly even Pyroluria. 

A number of studies have found that the gut flora of people with autism is quite different than that of healthy controls.  One recent study, Pyrosequencing study of fecal microflora of autistic and control children looked at the bacterial composition of microflora in 33 children with autism who have gastrointestinal symptoms compared to controls and found many significant differences, including:

"At the phylum level, Bacteroidetes and Firmicutes showed the most difference between groups of varying severities of autism. Bacteroidetes was found at high levels in the severely autistic group, while Firmicutes were more predominant in the control group. Smaller, but significant, differences also occurred in the Actinobacterium and Proteobacterium phyla. Desulfovibrio species and Bacteroides vulgatus are present in significantly higher numbers in stools of severely autistic children than in controls."

Desulfovibrio is a bacteria that causes problems with the metabolism of sulfur, which is a very common problem for people with autism.  It seems that the water supply may be one source of this bacteria.  If that is where it is coming from, then it would seem that colonization with this bacteria would be the result of an immune deficiency?

Some other recent studies have found that children with autism who also had gastrointestinal complaints had high levels of certain bacteria in gut biopsies, called Sutterella, that was not found in control subjects who did not have autism but did have GI complaints.  

Application of Novel PCR-Based Methods for Detection, Quantitation, and Phylogenetic Characterization of Sutterella Species in Intestinal Biopsy Samples from Children with Autism and Gastrointestinal Disturbances
"Here we describe an association between high levels of intestinal, mucoepithelial-associated Sutterella species and GI disturbances in children with autism. These findings elevate this little-recognized bacterium to the forefront by demonstrating that Sutterella is a major component of the microbiota in over half of children with autism and gastrointestinal dysfunction (AUT-GI) and is absent in children with only gastrointestinal dysfunction (Control-GI) evaluated in this study."

"In a previous study, we showed that a complex interplay exists between human intestinal gene expression for disaccharidases and hexose transporters and compositional differences in the mucoepithelial microbiota of children with autism and gastrointestinal disease (AUT-GI children) compared to children with GI disease but typical neurological status (Control-GI children). Significant compositional changes in Bacteroidetes, Firmicutes/Bacteroidetes ratios, and Betaproteobacteria in AUT-GI intestinal biopsy samples have been reported"

"The GI microbiota plays an essential role in physiological homeostasis in the intestine and periphery, including maintaining resistance to infection, stimulating immunological development, and perhaps even influencing brain development and behavior. Thus, disruption of the balanced communication between the microbiota and the human host could have profound effects on human health."

"In our previous metagenomic study, we found sequences corresponding to members of the family Alcaligenaceae in the class Betaproteobacteria that were present in ileal and cecal biopsy samples from 46.7% (7/15) of AUT-GI children...   Several members of Alcaligenaceae cause clinically relevant infections or are suspected opportunistic pathogens in humans and animals, including members of the genus Bordetella (including the human respiratory pathogens B. pertussis and B. parapertussis."

This is an earlier study done by the same researchers, the findings of which were the basis for the study referenced above.  Impaired carbohydrate digestion and transport and mucosal dysbiosis in the intestines of children with autism and gastrointestinal disturbances
"Reports of deficiencies in disaccharidase enzymatic activity and of beneficial responses to probiotic and dietary therapies led us to survey gene expression and the mucoepithelial microbiota in intestinal biopsies from children with autism and gastrointestinal disease and children with gastrointestinal disease alone. Ileal transcripts encoding disaccharidases and hexose transporters were deficient in children with autism, indicating impairment of the primary pathway for carbohydrate digestion and transport in enterocytes. Deficient expression of these enzymes and transporters was associated with expression of the intestinal transcription factor, CDX2. Metagenomic analysis of intestinal bacteria revealed compositional dysbiosis manifest as decreases in Bacteroidetes, increases in the ratio of Firmicutes to Bacteroidetes, and increases in Betaproteobacteria. Expression levels of disaccharidases and transporters were associated with the abundance of affected bacterial phylotypes. These results indicate a relationship between human intestinal gene expression and bacterial community structure and may provide insights into the pathophysiology of gastrointestinal disturbances in children with autism."

More research about Suterella and intestinal health and function:
Increased abundance of Sutterella spp. and Ruminococcus torques in feces of children with autism spectrum disorder
"We show that numbers of Sutterella spp. are elevated in feces of ASD children relative to controls, and that numbers of R. torques are higher in the children with ASD with a reported functional gastrointestinal disorder than those without such a disorder."

"A previous study by our group used quantitative real-time PCR (QPCR) to compare the abundance of a range of bacteria in feces of children with ASD, their siblings and community controls, and demonstrated a low relative abundance of Bifidobacterium spp. and the mucolytic bacterium Akkermansia muciniphila in children with ASD"  (Here is the study link:
Low relative abundances of the mucolytic bacterium Akkermansia muciniphila and Bifidobacterium spp. in feces of children with autism )

"Our results demonstrate that numbers of Sutterella are elevated in the feces of children with ASD relative to community controls. This confirms and builds on the findings of Williams et al."

"In this study we also extended our analysis of mucus-degrading bacteria in feces of ASD children, having previously shown a low abundance of the mucolytic bacterium A. muciniphila. We measured the abundances of R. torques and R. gnavus, both of which can degrade mucus and have been associated with GI disturbance. We have shown there is a trend of increased fecal numbers of R. torques in ASD children. This pattern of decreased numbers of A. muciniphila but increased numbers of R. torques in feces of ASD children is congruent with the pattern observed in the mucosa of adults with IBD. In the latter study it was also found that growth of A. muciniphila was inhibited by co-culture with MUC2, the predominant form of mucin in the large bowel, whereas this mucin augmented the growth of other bacteria such as R. torques. Although it is likely that the populations and activities of microbes that adhere to the mucus lining the large bowel may differ substantially from those in the feces, it is also likely that some changes in gut mucosal microbial populations are reflected in, and hence detectable in, feces. Changes in the amount of mucus produced may drive changes in mucus-degrading microbes in both the mucosa and in feces, as mucus can be incorporated into the fecal stream. Individuals with IBD or ASD may have changes in large bowel mucus production that could impact (or are a result of changes in) the mucosal barrier of the gut. Indeed, increased gut permeability has been reported in a subgroup of children with ASD."

Metagenomics revealed a correlation of gut phageome withautism spectrum disorder
“The public microbiota database of ASD and typically developing (TD) Chinese individuals were analyzed for phage protein-coding units (pPCU) to find any link between the phageome and ASD. The gut phageome of ASD individuals showed a wider diversity and higher abundance compared to TD individuals. The ASD phageome was associated with a significant expansion of Caudoviricetes bacteriophages. Phages infecting Bacteroidaceae and prophages encoded within Faecalibacterium were more frequent in ASD than in TD individuals. The expansion and diversification of ASD phageome can influence the bacterial homeostasis by imposing pressure on the bacterial communities. In conclusion, the differences of phages community in in ASD and TD can be used as potential diagnosis biomarkers of ASD. Further investigations are needed to verify the role of gut phage communities in the pathogenesis of ASD.”