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Sleeping Sickness Drug is Waking Up Autism Research

Brain colorsBy Teresa Conrick

For any who don´t know, I have a 24 year-old daughter who regressed into autism before her 3rd birthday.  Meg has the type of autism that does not make for an easy life.  She lost speech in 1995 and she is nonverbal still, and waves of difficult and painful medical symptoms then were to follow: cognitive decline, increasing GI issues, chronic bacterial infections and viral illnesses, seizures, and then a horrific autoimmune disorder called PANS [Pediatric Autoimmune Neuropsychiatric Syndrome] .

For years now, I have been following the research on the Microbiome as there are solid studies showing how dysfunctional it is in those with an autism diagnosis.  Studies like these represent hope for many families with very ill children and young adults:

Reduction of Ritualistic Behavior in a Patient with Autism Spectrum Disorder treated with Antibiotics: A Case Report 

Microbiota Transfer Therapy alters gut ecosystem and improves gastrointestinal and autism symptoms: an open-label study  

Combined oral fecal capsules plus fecal enema as treatment of late onset autism spectrum disorder in children: report of a small case series. 

Unexpected improvement in core autism spectrum disorder symptoms after long-term treatment with probiotics 

Age and severity may play a part in outcomes with our children as far as treatments.  I have now been following the research of Dr. Naviaux, still with the microbiome in mind, but also with a better understanding of its significance.  It seems that his research explains much of what I see in Meg, especially with the issues of the gut and brain.  You can watch this great video of a lecture by Dr. Naviaux, at a very recent TACA conference.  Thanks to them both!     

And in that lecture, Dr. Naviaux recommends that viewers read his study called, Metabolic features of the cell danger response  http://www.sciencedirect.com/science/article/pii/S1567724913002390.  Here are some excerpts:

The cell danger response (CDR) is an evolutionarily conserved cellular metabolic response that is activated when a cell encounters a chemical, physical, or microbial threat that could injure or kill the cell. Common microbial threats are viruses, bacteria, fungi, and parasites. Physical threats include heat, salt, or pH shock, or UV or ionizing radiation. Chemical forms of danger include heavy and trace metals like lead, mercury, cadmium, arsenic, and nickel, certain electrophilic aromatic chemicals like the plasticizer bisphenol A, the chemical flame retardants like the brominated diphenyl ethers (BDEs), and certain halogenated pesticides like chlorpyrifos and DDT. 

.... With the discovery that mitochondria represented the front lines in cellular defense and innate immunity, this connection between neurological setbacks and infection began to be understood....An important forcing variable in the control of chronic inflammation and the cell danger response is purinergic signaling...... Likewise, a large number of molecules have been synthesized since the 1850s as dyes, pesticides, drugs, and industrial chemicals. Many are polyaromatic and halogenated. These modern chemicals with conjugated ring systems, multiple double bonds, and delocalized π orbital electron clouds are highly electrophilic and will produce an electron steal within the cell that can also activate the CDR.......vitamin D metabolism is altered significantly by the CDR. .......Acute activation of the CDR stimulates the B6-dependent enzyme histidine decarboxylase to yield histamine....Histamine is also critical for mast cell and eosinophil function in allergy and the anti-parasite limb of innate immunity .....

...The chronic activation of the CDR alters both the physical habitat of the distal bowel and the availability of resources in the form of dietary nutrients. .... and to an increase in gluten sensitivity.  These and other factors combine to alter the permeability and species composition in the gut. Among children with ASD, this commonly leads to dysbiosis and alternating bouts of constipation and diarrhea. It also leads to changes in behavior that are a result of communication abnormalities between the enteric nervous system (ENS) that monitors the health and function of the microbiome, and the central nervous system (CNS). Restoring a sick microbiome is not as simple as adding back missing or underrepresented species. Both the physical habitat of the gut and the nutrient resources delivered must be durably changed in order to produce a durable change in the complex microbial ecosystem......Because the CDR is initially adaptive and coordinated by the close interplay of mitochondria and the cell, but becomes maladaptive once the environmental danger is gone, this can be referred to as “anachroadaptive mitocellular dysfunction”......Purinergic signaling appears to play an important role in sustaining the multifaceted metabolic features of the CDR. This observation led to the successful correction of all 16 of 16 multi-system, autism-like features in a classic animal model of ASD using antipurinergic therapy (APT).,,,,,An important caveat to APT is that if the physical, chemical, or biological trigger of the CDR has not been eliminated or neutralized, treatments designed to inhibit a persistent CDR may have mixed effects. 

Here is his 2017 paper causing much optimism for parents:

Low-dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical trial 

Connections that I would like to point out on this fascinating and hopeful research, since environmental factors have been shown to play a big part:

∗   Are there connections to Hannah Poling, the red-headed, little girl whom the world learned over ten years ago, to have regressed into autism due to Mitochondrial Dysfunction? 

∗   “ When the CDR is activated, the oxidizing intracellular conditions favor sequestration, toxic amounts of trace and heavy metals can be accumulated, and are not easily mobilized..”   

∗   “ Any trace or heavy metal that acts as an electrophile or sulfurophile in the cell will trigger a mitochondrial response that is similar to that of a viral infection, because metal electrophiles and replicating pathogens both divert and consume electrons. ”    

∗    “ The connection between neurodegenerative episodes and infection in mitochondrial disease was recognized and quantified in the early 2000s.”    

∗   “ Purinergic signaling appears to play an important role in sustaining the multifaceted metabolic features of the CDR. This observation led to the successful correction of all 16 of 16 multi-system, autism-like features in a classic animal model of ASD using antipurinergic therapy (APT).”  

∗  “ We found that disturbances in social behavior, novelty preference and metabolism are not permanent but are treatable with antipurinergic therapy (APT) ... single-dose APT with suramin acutely reverses these abnormalities, even in adults.      

As I said, much hope for our children here and I am thankful for that. If you would like to support this research, here is information to do just that.

Teresa Conrick is Science Editor for Age of Autism.



I wondered if suramin killed typan what ever and the other parasites that seem to bring on a sleeping sickness.

It does.

Interesting that it does so by causing the parasite to lose energy. ATP.

We don't have 20 years, for this might work, we do all the science, and do it right.
I don't mean me and my family don't have 20 years. which we don't.

I did mean we don't have 20 years as in the human race. I see it is knocking at our door now in all kinds of social interactions of our society.


I am looking at the treatment for sleeping sickness parasite -- trypanosomiasis

There are a total five different drugs are used for the treatment of sleeping sickness.

Drugs used in first stage treatment:

Pentamidine: discovered in 1940, used for the treatment of the first stage of T.b. gambiense sleeping sickness. Despite non-negligible undesirable effects, it is in general well tolerated by patients.
Suramin: discovered in 1920, used for the treatment of the first stage of T.b. rhodesiense. It provokes certain undesirable effects, including urinary tract and allergic reactions.
Drugs used in second stage treatment:

Melarsoprol: discovered in 1949, it is used for the treatment of both gambiense and rhodesiense infections. It is derived from arsenic and has many undesirable side effects, the most dramatic of which is reactive encephalopathy (encephalopathic syndrome) which can be fatal (3% to 10%). An increase in resistance to the drug has been observed in several foci, particularly in central Africa. It is currently recommended as first-line treatment for the rhodesiense form, and as second-line for the gambiense form.
Eflornithine: this molecule, less toxic than melarsoprol, was registered in 1990. It is only effective against T.b. gambiense. The regimen is complex and difficult to apply.
Nifurtimox: A combination treatment of nifurtimox and eflornithine was introduced in 2009. It simplifies the use of eflornithine by reducing the duration of treatment and the number of IV perfusions, but unfortunately it has not been studied for T.b. rhodesiense. Nifurtimox is registered for the treatment of American trypanosomiasis but not for human African trypanosomiasis. Nevertheless, after safety and efficacy data provided by clinical trials, its use in combination with eflornithine has been included in the "WHO List of Essential Medicines" and is currently recommended as first-line treatment for the gambiense form


I looked at his video last night. Darn I fell asleep. These days are sometimes just too hard.
So, the parasite found in Africa, that causes sleeping sickness; works in the same way as what is happening in autism? This electron capture bad thing; can also be metals and benzene rings?
This is happening inside the cells or outside the cells? I did not get that part?

He is using a very old drug. It has been around a while. I don't know what the out come is for those in Africa that had sleeping sickness and took this drug? Did they get completely better, or very much improve and not have to take this drug again?

He zeros in on ATP. I am very familiar with how ATP is made in the mitochondria. Did you know that we produce three times our body weight in ATP each day? I think I am remembering that right? It was in some book some where. It is all starting to run together. But the receptors of ATP is that what is messed up?

We have one relative that now has mythensis gravis, and it is not genetic but had an environmental trigger. That has to do with ATP. I was thinking maybe she has an allergy to ATP. Goodness knows my husband has his diagnosis of a mitochondria production of ATP.

But they said it was not producing, that the pathway that produced the most ATP was messed up.


One can not have science
without the truth

Thank you Ms Conrick
for always telling the truth


Please see these links for (I believe) another piece of the puzzle:


"The measurements of bacterial radio waves were published in 2009 by Luc Montagnier, who won the Nobel Prize for medicine in 2008 for the discovery of HIV. "



Naviaux had remarked during his TACA presentation that depending on funding and additional trials, actual treatment with Suramin or possibly another medication was (if I remember correctly) 15-20 years away. Autism Speaks originally funded his work in this area, the most promising treatment to date I believe, in the form of a pill/infusion anyway. Why the hell are they not continuing to fund his research? Interesting how when his first studies were done the media reported on it and now silence. Probably something to do with the fact his research proves autism is an immune system disorder. Time to start making some noise on this particular subject.

Angus Files

I think mercury is the blame for it maybe the winged messenger will tell us one day.

Pharma For Prison


bob moffit

Teresa asks:

"Are there connections to Hannah Poling, the red-headed, little girl whom the world learned over ten years ago, to have regressed into autism due to Mitochondrial Dysfunction?"

Please correct me if I am wrong .. but .. TEN years AFTER Hannah Poling .. it is my understanding that infants and children are STILL receiving the full schedule of recommended and approved vaccines .. without ANY precautionary testing as to their possible Mitochondrial Dysfunction.

It should be obvious to any and all .. the scientific likelihood of manufacturing a "one size fits all vaccine" is PREPOSTEROUS. After all ... just like fingerprints ... each and every child has their own ... (Microbiome) .. unique development of their immune system .. which means the timing and exposure of dangerous "toxic amounts of trace and heavy metals" ... at varying times and in various amounts .. are far more than likely to have a PROFOUND affect on the child whose Mitochondria is deficient.

Trust me .. just like "one size fits all vaccines" ... if mandatory infant car seats and bike helmets were NOT ADJUSTABLE to PHYSICALLY fit each and every infant and child who are required to utilize them ... THOSE PRODUCTS WOULD SOON PROVE TO BE UNSAFE!

Obviously .. parents can SEE with their own eyes whether or not the car seat or bike helmet physically fits THEIR CHILD .. but .. those same parents have absolutely no way to observe whether or not their child can TOLERATE a recommended and approved vaccine.


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