We have collected many research articles to show that the toxins found
in microorganisms play an important role in the suspected causes of ASD,
in particular, lipopolysaccharide ( LPS) the bacterial toxins from gram
negative bacteria that inhabit the guts of autistic children.
toxicity works synergistically with mercury and other heavy metal
poisonings to expand damage. These heavy metals increase harm from
In addition, LPS decreases glutathione
levels making it even more difficult for the body to detoxify heavy
One explanation for why symptoms of mercury are so similar to the
symptoms of LPS could be the fact that mercury inhibits carbohydrate
absorption in the gut. Unabsorbed food does not get into the blood
stream quickly; when it remains in the gut, it becomes available as a
food supply for bacteria. Consequently, gram negative bacteria multiply
and produce LPS.  This raises a strong suspicion that some of the
symptoms commonly attributed to mercury could be directly caused by
LPS and only indirectly by mercury.
LPS also renders toxins from Candida Albicans more damaging.
The poisonous effects of LPS are so potent that they produce
symptoms of autism even without the help of Candida Albicans and heavy
collected experiments on the following website involve laboratory mice
injected with only LPS and exhibiting the same symptoms as
those in ASD.
LPS induces a depressive syndrome, characterized by anhedonia,
anorexia, body weight loss, and reduced locomotor, exploratory, and
social behavior. This result has been replicated so many times by
different research studies that the names, "Sickness Behavior" and "Endotoxemia" are now
applied to this condition. 
The mission of this website is to collect and display links to some of the
available research articles from
PubMed, a service from the National Library of Medicine and the National
Institute of Health, that link LPS to the varied and diverse symptoms
We were able to find and collect experiments for almost every possible neurological and biological
symptom of ASD in order to prove that
most symptoms of ASD, have a corresponding experiment
on Medline that proves each is a symptom of LPS toxicity.
The articles on this website are just a tiny fraction of the available research The amount of evidence is overwhelmoing, for example, performing a search for "hippocampus lps", in PubMed will retrieve 222 citations.
The number of similarities between ASD and LPS toxicity is sufficiently
impressive to demand attention and cannot be ignored. The
following are symptoms of LPS poisoning; these symptoms are also found in children with autism:
Reductions in oligodendrocyte or myelin markers
A marked cerebral cytokine response
White matter injury
Changes in amygdala
Change in dopamine and serotonin levels
Reduction of blood flow to the brain
Changes in blood-brain barrier permeability for large (protein)
Increased the number of pyramidal and granular cells in the
EMOTIONS AND BEHAVIOR
Reduction in social behavior
Lack of social interaction
Increase in addiction
Lack of exploratory behavior
Breakage and depletion of microvilli
The tight junctions widen and become disrupted.
IBS and IBD
Disrupted Intestinal Transit
LPS is linked to the problems of gluten,soy and dairy
in ASD children
Increase in TNF alpha.
Increases in certain NK cells and monocytes
Increases in lymphocytes
Low Levels of Thyroid
Low Levels of Glutathione
Low Levels of Amino Acids
Impairment of Bile Flow
Increasing the Number of Viable Candida Albicans
An increase in pain sensitivity
Researchers at the UC Davis M.I.N.D. Institute found clear differences
responses between autistic children and neurotypical children following
exposure to LPS, bean lectin and bacterial agents. At the Institute
this was discovered to be a major and important difference
between children with ASD and typical children.
"Lipopolysaccharide (LPS) is localized at the exterior leaflet of the
outer membrane and serves as the major surface component of the
bacterial cell envelope. This remarkable glycolipid is essential to
virtually all Gram-negative organisms and represents one of the
conserved microbial structures responsible for activation of the innate
immune system. For these reasons, the structure, function, and
biosynthesis of LPS has been an area of intense research."
The majority of the research articles involve mice or humans displaying
of toxemia after being given an injection of LPS. Another method to
the important influence of bacterial toxins
is to observe the changes in ASD children after removal of the
neurotoxin-producing bacteria. Both Vancomycin and the Specific
Carbohydrate Diet (SCD) are
treatments for removal of bacteria. Both treatments produce a
decrease in the symptoms of ASD. However, the changes from vancomycin
only short term because the bacteria develop a resistance to the
medication. Changes from SCD diet are more powerful
because they are long lasting. Even adults with ASD who live in group
homes have been shown to lose many of their symptoms after being on the
now also eliminates beans during the early months of the diet and
encourages parents to only use beans later provided there are no adverse
UC Davis M.I.N.D. Institute reports in its findings concerning the
autistic children to LPS, bacterial agents and lectin from beans
lead to significant advances in the early detection, prevention and
treatment of this complex neurological disorder."
We are in total agreement, and offer as our own evidence, scientific
articles and many positive results from using a diet that eliminates
neurotoxin-producing bacteria and fosters intestinal healing.
In view of the research, we have to consider Lipopolysaccharide (LPS)
a poison, as toxic as mercury
and other heavy metals, LPS has drastic consequences for those in the
ASD Community. Fortunately, dramatic improvements may result
after its removal.
Increasing awareness of LPS to doctors, researchers and parents, will
hopefully result in an increase in recovery rates for autism.
The links on the upper side of this website provide
comprehensive research about LPS from around the world.
Rumbeiha WK, Fitzgerald SD, Braselton WE, Roth RA, Kaneene JB:
Potentiation of mercury-induced nephrotoxicity by endotoxin in the Sprague-Dawley rat. Toxicology. 2000 Aug 21;149(2-3):75-87.
Altered glutathione homeostasis in animals prenatally exposed to lipopolysaccharide. Neurochem Int. 2007 Mar;50(4):671-80. Epub 2007 Jan 13.
Read the articles in the "Treatments for LPS" section of this website
Akagawa G, Abe S, Yamaguchi H.
Mortality of Candida albicans-infected mice is facilitated by superinfection of Escherichia coli or administration of its lipopolysaccharide. J Infect Dis. 1995 Jun;171(6):1539-44.
 Singal A,
Green tea (Camellia sinensis) extract ameliorates endotoxin induced sickness behavior and liver damage in rats. Phytother Res. 2006 Feb;20(2):125-9.
R. YIRMIYA, Y. POLLAK, M. MORAG, A. REICHENBERG, O. BARAK, R. AVITSUR, Y. SHAVIT, H. OVADIA, J. WEIDENFELD, A. MORAG, M. E. NEWMAN, T. POLLM�CHER (2000)
Illness, Cytokines, and Depression
Annals of the New York Academy of Sciences 917 (1), 478�487.
Reversible inactivation of the dorsal vagal complex blocks lipopolysaccharide-induced social withdrawal and c-Fos expression in central autonomic nuclei. Brain Behav Immun. 2004 Mar;18(2):123-34.
Link to the anouncement from the M.I.N.D. Institute.
Trent, M. Stephen1; Stead, Christopher M.1; Tran, An X.1; Hankins, Jessica V.(2006).
Diversity of endotoxin and its impact on pathogenesis. Journal of Endotoxin Research, Volume 12, Number 4, August 2006, pp. 205-223(19)
Autism: Effective Biomedical Treatments (Have We Done Everything We Can For This Child? Individuality In An Epidemic) by Rimland, Ph.D. Bernard (Introduction), M.D. Sidney Baker (Author), Ph.D. Jon Pangborn (Author) Boston DAN! April 2005 edition. Page 24