Autism successfully treated - latent Lyme disease the culprit - energy levels lifted

I'll press on a bit...tight junctions also prevent the passage of water; looser junctions don't.

Around the time of my onset, about 17 years ago, I spent a night at a friend's house. During the night, I felt a rapidly-growing itching, and a sensation that I can only describe in exactly the same way that many Morgellon's sufferers describe their onset event: like millions of tiny insects crawling around just under the skin. The sensation spread rapidly across my whole body within minutes. It was very weird and I've never felt anything like it, before or since.

It was around this time that my symptoms began - and unfortunately I'm unable to place the events in sequence because they didn't seem so important then as they do now. But amongst the first of what I now recognise as the onset of my symptoms was the bizarre night-sweats. I'm not certain whether they came after the event I just described. (I also got persistent fungal infections soon afterwards, starting with athlete's foot, which I'd never had before...could tight junctions be significant in protecting against fungal infection?)

But noting the function of tight junctions in preventing water from passing through, and noting that whenever my itching and gut issues worsen I get night sweats, and a return of the same sickly-sweet-smelling sweat that lingers for ages on towels...I'm wondering whether this sweat is related to some liquid passing through tight junctions that wouldn't normally get through. A bit more tenuous than the above observations perhaps...but I'm also reminded that my sister (also a long-term sufferer of "IBS/PVFS/CFS") now reports problems with 'water-retention'...could that phenomenon also be related to the function of tight junctions I wonder?

Any information about tight junctions, I'm interested...perhaps the subject deserves a separate thread?

 

In well studied ones like HIV this increased gut permeability and bacterial translocation is well known and improves on antiretrovirals.

One of the main entry receptors for enteroviruses is CAR, which is closely linked to tight junction mechanisms. I once asked one enterovirus researcher about this being a factor in leaky gut, she said it hadn't been studied but quite possible.

Probiotics and glutamine have been well studied, some other things also promising. I will post the list below.

 

I guess this might be the same as diets and supplements used by some people with autism?
If so then there would be lots of info about this on autism websites and forums.

I guess that makes sense, if a leaky tight junction barrier lets water through.

It definitely deserves a separate thread but there are probably already threads about leaky gut and leaky blood-brain barrier, so it might be worth looking at those, to see if we are duplicating?

 

Agents that reduce gut permability and bacterial translocation:


Probiotics lots of positive studies on various ones

Glutamine lots of positive studies

Antioxidants various ones
(ALA hasnt been studied in gut but did reduce BBB permeability in EAE!)

Arginine
http://www.ncbi.nlm.nih.gov/pubmed/19660909

Bovine colostrum
http://www.ncbi.nlm.nih.gov/pubmed/19298194

vasoactive intestinal peptide
http://www.ncbi.nlm.nih.gov/pubmed/19661153

Growth hormone
http://www.ncbi.nlm.nih.gov/pubmed/14975214

Butyrate/prebiotics
We speculate that prebiotics, the substrate for butyrate synthesis, is a valuable prophylaxis in the regulation of epithelial permeability and could be of benefit in preventing relapses in IBD http://www.ncbi.nlm.nih.gov/pubmed/20024905

Adrenomedullin
Citruline
Antiretrovirals reduce HIV-induced gut permeability



Factors contributing/inducing permeability:

infections, toxins, mast cell activation !!, surgery (organ transplants, abdomen surgery), temperature increase (fever?), alcohol/liver failure, trauma, stress, nitric oxide, pancreatitis, burn injury, traumatic head injury, radiation, COX-2 inhibition (ibuprofen?)

high protein milk formulas in neonates alters gut permeability in later life http://www.ncbi.nlm.nih.gov/pubmed/21573022


Now a really interesting one: GLUTEN sensitivity!
Increased bacterial translocation in gluten-sensitive mice is independent of small intestinal paracellular permeability defect
http://www.ncbi.nlm.nih.gov/pubmed/21822909



Exacerbation of intestinal permeability in rats after a two-hit injury: burn and Enterococcus faecalis infection.
http://www.ncbi.nlm.nih.gov/pubmed/15640640

Persistent epithelial dysfunction and bacterial translocation after resolution of intestinal inflammation
http://www.ncbi.nlm.nih.gov/pubmed/11518675

Significance of nervous system in inflammatory disease of the gut
http://www.ncbi.nlm.nih.gov/pubmed/22308741

 

Gosh Natasa, you've been doin your homework!

Thanku for the info.

 

A good review article on endotoxins (though it takes a while to load and is 9 years out of date):

http://www.mendeley.com/research/innate-immune-sensing-roots-story-endotoxin/#page-1

 

Not sure if this has been posted here before - a very recent paper by Lipkin, Hornig et al. Not looking at permeability issues but links in to this thread

Impaired Carbohydrate Digestion and Transport and Mucosal Dysbiosis in the Intestines of Children with Autism and Gastrointestinal Disturbances

Gastrointestinal disturbances are commonly reported in children with autism, complicate clinical management, and may contribute to behavioral impairment. 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.


The paper is very long and looks into several aspects, this one is very interesting and probably relevant to leaky gut discussion:

Associations between gene expression, bacterial abundance, and food allergies and other comorbid atopic manifestations
A National Survey of Children's Health, performed under the auspices of the Centers for Disease Control, reported that parents of autistic children reported more allergy symptoms than control children, and food allergies were the most prevalent complaint [39]. Parental reports of food allergies (FA) in our cohort were reported with similar frequency in AUT-GI (67%) and Control-GI (71%) children. Milk-related (MA) and wheat-related (WA) allergies were the most commonly reported allergies in both groups.
...
Stratification by any FA revealed a significant effect for levels of GLUT2, ileal and cecal Firmicutes, ileal and cecal ratios of Firmicutes to Bacteroidetes, and cecal Betaproteobacteria (Table 5). No effect was observed for the levels of Bacteroidetes, which were significantly reduced in AUT-GI children independent of FA status.

Stratification by MA status revealed even more significant effects (Table 6). Significant effects were observed for MGAM, GLUT2, and CDX2 expression, as well as ileal and cecal ratios of Firmicutes to Bacteroidetes, and ileal and cecal Beta-proteobacteria. Additional trends were observed for SI expression and ileal and cecal Firmicutes. No effect was observed for the levels of Bacteroidetes, which were significantly reduced in AUT-GI children independent of MA status.

Stratification by WA status was associated with a significant effect only for cecal levels of Firmicutes, though this effect was highly significant [AUT(+WA) vs. AUT(?WA): Mann-Whitney, p-value = 0.008], and the cecal ratio of Firmicutes to Bacteroidetes (Table 7).

These results suggest that changes in the expression of some disaccharidases and transporters and CDX2, as well as changes in the abundance of some bacterial phylotypes, are significantly associated with reported FA, especially MA.


it goes on ...



full paper
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3174969/?tool=pubmed


p.s. my son had eczema as a toddler, it wasn't responding to rx topical creams but disappeared overnight after removing gluten/wheat from diet

 

Hi Natasa,

Yeah, I posted this study at my post #7.

I have put the others from that post below, instead of just the links. I think they are quite interesting. I have included some more, including a small study on intestinal permeability in autism and also carbohydrate malabsorption. This would then be a good working theory of bacterial overgrowth, using the carbohydrates.

Abnormal intestinal permeability in children with autism.D'Eufemia P, Celli M, Finocchiaro R, Pacifico L, Viozzi L, Zaccagnini M, Cardi E, Giardini O.
SourceInstitute of Pediatrics, La Sapienza University of Rome, Italy.

Abstract

We determined the occurrence of gut mucosal damage using the intestinal permeability test in 21 autistic children who had no clinical and laboratory findings consistent with known intestinal disorders. An altered intestinal permeability was found in 9 of the 21 (43%) autistic patients, but in none of the 40 controls. Compared to the controls, these nine patients showed a similar mean mannitol recovery, but a significantly higher mean lactulose recovery (1.64% +/- 1.43 vs 0.38% +/- 0.14; P < 0.001). We speculate that an altered intestinal permeability could represent a possible mechanism for the increased passage through the gut mucosa of peptides derived from foods with subsequent behavioural abnormalities.



Alterations of the intestinal barrier in patients with autism spectrum disorders and in their first-degree relatives.
de Magistris L, Familiari V, Pascotto A, Sapone A, Frolli A, Iardino P, Carteni M, De Rosa M, Francavilla R, Riegler G, Militerni R, Bravaccio C.
SourceDepartment Magrassi-Lanzara, Gastroenterology, Second University of Naples, Italy. laura.demagistris@unina2.it

Abstract

OBJECTIVES: Intestinal permeability (IPT) was investigated in patients with autism as well as in their first-degree relatives to investigate leaky gut hypothesis. Faecal calprotectin (FC) was also measured in patients with autism, either with or without gastrointestinal symptoms, and in their first-degree relatives.

PATIENTS AND METHODS: IPT results, assessed by means of the lactulose/mannitol test, were compared with adult and child controls and with FC values.

RESULTS: A high percentage of abnormal IPT values were found among patients with autism (36.7%) and their relatives (21.2%) compared with normal subjects (4.8%). Patients with autism on a reported gluten-casein-free diet had significantly lower IPT values compared with those who were on an unrestricted diet and controls. Gastrointestinal symptoms were present in 46.7% of children with autism: constipation (45.5%), diarrhoea (34.1%), and others (alternating diarrhoea/constipation, abdominal pain, etc: 15.9%). FC was elevated in 24.4% of patients with autism and in 11.6% of their relatives; it was not, however, correlated with abnormal IPT values.

CONCLUSIONS: The results obtained support the leaky gut hypothesis and indicate that measuring IPT could help to identify a subgroup of patients with autism who could benefit from a gluten-free diet. The IPT alterations found in first-degree relatives suggest the presence of an intestinal (tight-junction linked) hereditary factor in the families of subjects with autism.



Real-time PCR quantitation of clostridia in feces of autistic children.
Song Y, Liu C, Finegold SM.
SourceResearch Service, VA Medical Center West Los Angeles, Los Angeles, California 90073, USA. yulis1@yahoo.com

Abstract
Based on the hypothesis that intestinal clostridia play a role in late-onset autism, we have been characterizing clostridia from stools of autistic and control children. We applied the TaqMan real-time PCR procedure to detect and quantitate three Clostridium clusters and one Clostridium species, C. bolteae, in stool specimens. Group- and species-specific primers targeting the 16S rRNA genes were designed, and specificity of the primers was confirmed with DNA from related bacterial strains. In this procedure, a linear relationship exists between the threshold cycle (CT) fluorescence value and the number of bacterial cells (CFU). The assay showed high sensitivity: as few as 2 cells of members of cluster I, 6 cells of cluster XI, 4 cells of cluster XIVab, and 0.6 cell of C. bolteae could be detected per PCR. Analysis of the real-time PCR data indicated that the cell count differences between autistic and control children for C. bolteae and the following Clostridium groups were statistically significant: mean counts of C. bolteae and clusters I and XI in autistic children were 46-fold (P = 0.01), 9.0-fold (P = 0.014), and 3.5-fold (P = 0.004) greater than those in control children, respectively, but not for cluster XIVab (2.6 x 10(8) CFU/g in autistic children and 4.8 x 10(8) CFU/g in controls; respectively). More subjects need to be studied. The assay is a rapid and reliable method, and it should have great potential for quantitation of other bacteria in the intestinal tract.


Gastrointestinal microflora studies in late-onset autism.
Finegold SM, Molitoris D, Song Y, Liu C, Vaisanen ML, Bolte E, McTeague M, Sandler R, Wexler H, Marlowe EM, Collins MD, Lawson PA, Summanen P, Baysallar M, Tomzynski TJ, Read E, Johnson E, Rolfe R, Nasir P, Shah H, Haake DA, Manning P, Kaul A.
SourceInfectious Diseases Section, Veterans Affairs Medical Center, West Los Angeles, CA, USA. sidfinegol@aol.com

Abstract
Some cases of late-onset (regressive) autism may involve abnormal flora because oral vancomycin, which is poorly absorbed, may lead to significant improvement in these children. Fecal flora of children with regressive autism was compared with that of control children, and clostridial counts were higher. The number of clostridial species found in the stools of children with autism was greater than in the stools of control children. Children with autism had 9 species of Clostridium not found in controls, whereas controls yielded only 3 species not found in children with autism. In all, there were 25 different clostridial species found. In gastric and duodenal specimens, the most striking finding was total absence of non-spore-forming anaerobes and microaerophilic bacteria from control children and significant numbers of such bacteria from children with autism. These studies demonstrate significant alterations in the upper and lower intestinal flora of children with late-onset autism and may provide insights into the nature of this disorder.

Short-term benefit from oral vancomycin treatment of regressive-onset autism.
Sandler RH, Finegold SM, Bolte ER, Buchanan CP, Maxwell AP, Visnen ML, Nelson MN, Wexler HM.
SourceSection of Pediatric Gastroenterology and Nutrition, Rush Children's Hospital, Rush Medical College, Chicago, IL 60612, USA. rushstudy@aol.com

Abstract
In most cases symptoms of autism begin in early infancy. However, a subset of children appears to develop normally until a clear deterioration is observed. Many parents of children with "regressive"-onset autism have noted antecedent antibiotic exposure followed by chronic diarrhea. We speculated that, in a subgroup of children, disruption of indigenous gut flora might promote colonization by one or more neurotoxin-producing bacteria, contributing, at least in part, to their autistic symptomatology. To help test this hypothesis, 11 children with regressive-onset autism were recruited for an intervention trial using a minimally absorbed oral antibiotic. Entry criteria included antecedent broad-spectrum antimicrobial exposure followed by chronic persistent diarrhea, deterioration of previously acquired skills, and then autistic features. Short-term improvement was noted using multiple pre- and post-therapy evaluations. These included coded, paired videotapes scored by a clinical psychologist blinded to treatment status; these noted improvement in 8 of 10 children studied. Unfortunately, these gains had largely waned at follow-up. Although the protocol used is not suggested as useful therapy, these results indicate that a possible gut flora-brain connection warrants further investigation, as it might lead to greater pathophysiologic insight and meaningful prevention or treatment in a subset of children with autism.



Differences between the gut microflora of children with autistic spectrum disorders and that of healthy children.
Parracho HM, Bingham MO, Gibson GR, McCartney AL.
SourceFood Microbial Sciences Unit, School of Food Biosciences, The University of Reading, Whiteknights, PO Box 226, Reading RG6 6AP, UK.

Abstract
Children with autistic spectrum disorders (ASDs) tend to suffer from severe gastrointestinal problems. Such symptoms may be due to a disruption of the indigenous gut flora promoting the overgrowth of potentially pathogenic micro-organisms. The faecal flora of patients with ASDs was studied and compared with those of two control groups (healthy siblings and unrelated healthy children). Faecal bacterial populations were assessed through the use of a culture-independent technique, fluorescence in situ hybridization, using oligonucleotide probes targeting predominant components of the gut flora. The faecal flora of ASD patients contained a higher incidence of the Clostridium histolyticum group (Clostridium clusters I and II) of bacteria than that of healthy children. However, the non-autistic sibling group had an intermediate level of the C. histolyticum group, which was not significantly different from either of the other subject groups. Members of the C. histolyticum group are recognized toxin-producers and may contribute towards gut dysfunction, with their metabolic products also exerting systemic effects. Strategies to reduce clostridial population levels harboured by ASD patients or to improve their gut microflora profile through dietary modulation may help to alleviate gut disorders common in such patients.




Intestinal disaccharidase activity in patients with autism: effect of age, gender, and intestinal inflammation.
Kushak RI, Lauwers GY, Winter HS, Buie TM.
SourceHarvard Medical School, Boston, MA, USA. kushak.rafail@mgh.harvard.edu

Abstract
Intestinal disaccharidase activities were measured in 199 individuals with autism to determine the frequency of enzyme deficiency. All patients had duodenal biopsies that were evaluated morphologically and assayed for lactase, sucrase, and maltase activity. Frequency of lactase deficiency was 58% in autistic children ? 5 years old and 65% in older patients. As would be expected, patients with autism at age 5 > years demonstrated significant decline in lactase activity (24%, p = .02) in comparison with ? 5 years old autistic patients. Boys ? 5 years old with autism had 1.7 fold lower lactase activity than girls with autism (p = .02). Only 6% of autistic patients had intestinal inflammation. Lactase deficiency not associated with intestinal inflammation or injury is common in autistic children and may contribute to abdominal discomfort, pain and observed aberrant behavior. Most autistic children with lactose intolerance are not identified by clinical history.

Gastrointestinal abnormalities in children with autistic disorder.
Horvath K, Papadimitriou JC, Rabsztyn A, Drachenberg C, Tildon JT.
SourceDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, USA.

Abstract
OBJECTIVES: Our aim was to evaluate the structure and function of the upper gastrointestinal tract in a group of patients with autism who had gastrointestinal symptoms.

STUDY DESIGN: Thirty-six children (age: 5.7 +/- 2 years, mean +/- SD) with autistic disorder underwent upper gastrointestinal endoscopy with biopsies, intestinal and pancreatic enzyme analyses, and bacterial and fungal cultures. The most frequent gastrointestinal complaints were chronic diarrhea, gaseousness, and abdominal discomfort and distension.

RESULTS: Histologic examination in these 36 children revealed grade I or II reflux esophagitis in 25 (69.4%), chronic gastritis in 15, and chronic duodenitis in 24. The number of Paneth's cells in the duodenal crypts was significantly elevated in autistic children compared with non-autistic control subjects. Low intestinal carbohydrate digestive enzyme activity was reported in 21 children (58.3%), although there was no abnormality found in pancreatic function. Seventy-five percent of the autistic children (27/36) had an increased pancreatico-biliary fluid output after intravenous secretin administration. Nineteen of the 21 patients with diarrhea had significantly higher fluid output than those without diarrhea.

CONCLUSIONS: Unrecognized gastrointestinal disorders, especially reflux esophagitis and disaccharide malabsorption, may contribute to the behavioral problems of the non-verbal autistic patients. The observed increase in pancreatico-biliary secretion after secretin infusion suggests an upregulation of secretin receptors in the pancreas and liver. Further studies are required to determine the possible association between the brain and gastrointestinal dysfunctions in children with autistic disorder.

 

more from Montagnier

http://francisworldinsideout.wordpr...-will-follow-the-steps-of-jacques-benveniste/

some interesting discussion in comments below the article

 

Just going back to the original post: My doctor told me there have been three studies published now, one in the US, one in Canada and one in Scotland, which tested hundreds of autistic children and found that 80 percent in one study and 90 percent in another, had Lyme disease. Unfortunately I cannot find these studies published freely on the internet. They have been presented at the ILADS conferences worldwide over the last few years.

The main website for parents of kids with Lyme induced autism is here:

http://www.lymeinducedautism.com/

We parents who have found our kids became autistic because of Lyme disease are like a tiny secret society. I keep posting this on Facebook, I tell all my friends, I try to spread the word, but it still feels as if we are in a secret society like the Freemasons, who share a powerful secret that outsiders know nothing about.

Where I live in Sicily I have had four families with autistic children approach me over the last 18 months, because word is spreading about how I cured my autistic son. I told all of them to get their children tested for Lyme disease, and three of the four came up positive. The last one still has not tested, the mother is very strange and I don't understand why she doesn't want to go ahead with the test (ah, another story).
The sickest little boy was severely autistic, he had no speech and made no human contact with his parents. He's been on antibiotics for 6 months now and is starting to speak. He often approaches his father with a toy in his hand and asks him to play. His terrible gut problems are still there but slightly improving.
I desperately wish I could reach all the autistic children and tell their parents how to help them.

The extreme itching that an autistic child suffered, mentioned in an earlier post, and which was relieved by antibiotics, would have been bartonella, which is the commonest Lyme disease co-infection, also transmitted by ticks. The bacteria reproduce under the skin and then migrate into the body. They have a five day lifecycle and the itching reaches a climax every five days because of this. One of the so-called "self harm" behaviours common in autistic children is to scratch themselves till they bleed; I have bartonella, and I have done that too.

 

And, by quite a coincidence, here's a drug that might address the issues we've been talking about:

http://phoenixrising.me/forums/show...cure-treatment-for-Leaky-Gut-(PLoS-ONE-study)

 

I really hope that this puzzle starts solving itself now.

 

Success in TREATING AUTISM WITH ANTIBIOTICS

Luc Montagnier, an HIV pioneer, is now studying an infectious link to autism in France.
Results are amazing -- 4 of 5 children with autism (out of 200 followed) have dramatic improvement with antibiotics.


[video=youtube;yOno_2m_8LY]http://www.youtube.com/watch?feature=player_embedded&v=yOno_2m_8LY[/video]

 

F I N A L L Y!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

 

Just marvellous !

 

Prof Luc Montagnier is also an Honorary Member of the European Society for ME (ESME):
http://esme-eu.com/home/announcemen...ins-esme-as-honorary-member-article446-6.html

 

Wow, that's serious class. I was doing my degree when HTLV-III/HIV research was taking off and he's about as impressive as it gets in the world of science.

 

The thing that bothers me is that they keep stopping treatment when the child improves and then re-start again when he regresses.
That is all wrong, and just leads to antibiotic resistance. You have to keep going relentlessly till you have eliminated the infection fully.
They have been curing Lyme induced autism with antibiotics for many years in America. It usually takes 3 to 8 years of solid antibiotics non stop to eradicate it and let the child live a normal adult life.

My source for these comments is here, BTW
http://www.ilads.org/media/videos/videos_jones.php

 

Montagnier will be presenting on this topic in September at UK autism conference

http://www.treatingautism.co.uk/events/565/save-the-dates-treating-autism-conference-2012/

also Jeremy Nicholson should be very interesting...

btw De Meirleir will be speaking on GcMAF in general at the same conference, and Dr Bradstreet will also cover GcMAF but more autism-specific (he is using ultra-low doses).

 

I wish De Merileir would get struck off for malpractise.
GcMaf causes atrocious harm to people with Lyme disease. I have a friend (I met her in KDMs waiting room) to whom he prescribed it for CFS, after failing to perform a proper test for Lyme disease - she has Lyme disease but he didn't know it. She was functioning about level 7 on the 1-10 scale, and his treatment reduced her to bedbound at level 1. She was hospitalised and at this point he wanted nothing more to do with her - he became arrogant, disinterested and downright verbally abusive; which is exactly how he treated me when his treatment made me worse not better.

I was dumped off his patient list and treated disgracefully a year before she was and I kept asking myself why? What had I done to offend him so deeply? Before he put her on GcMaf she was improving, and he was very friendly to her. Then when she regressed seriously, he suddenly changed to her as well, and I realised that my only offence had been to get very sick on his therapy.

Then he goes off to conferences and says "80 percent of his patients have made great improvements" - that statistic is only true because he gets on the phone to all the ones who become worse and insults them (literally) until they go away and are not his patients any more!
Then they go to actual, competent doctors who conduct impartial research into Lyme disease, who mop up his messes.