Prelude to my upcoming Autism One lecture on the INCREDIBLY important ENDOCANNABINOID SYSTEM


Teri from Autism One Radio interviews Dr Bradstreet about the Autism Nexus.  Listen here by clicking on the link below.

See you at Autism One in Chicago.

In Defense of – why knowing your genome is important

Up until November of 2013 the controversial website offered people the opportunity to get genomic insights to their past and their possible future – at least their future vulnerabilities.  After 2 years of back and forth communication wherein it seems 23andMe was trying (unsuccessfully) to convince the FDA that people had the right to genomic information the FDA issued a cease and desist order and now 23andMe states this on their homepage: “23andMe provides ancestry-related genetic reports and uninterpreted raw genetic data. We no longer offer our health-related genetic reports.” 

The price of the testing dropped dramatically and is now only $99 for a salivary genomic test.  The problem is that unless you actually care what percentage of your ancestral DNA comes from what continent or how much residual Neanderthal your parents contributed to you, the raw data is merely a huge outpouring of A,T,C G data (nucleic acid pairs) which even a competent geneticist would find daunting without the aid of serious computer databases.  But therein lies its wonder – we do have access to amazing databases which offer us glimpses into the rapidly expanding arena of medical genomics and personalized health care. 

Enter in a support industry growing up around 23andMe like livewello, which offers an app for downloading all those ATCG codes and converting them to more easily understood labels, like MTHFR – a gene with common single nucleotide substitutions which may result in dramatic reductions in its enzyme’s ability to methylate folate (a completely treatable genetic risk factor for heart disease, certain cancers and autism). 



The livewello gene app for 23andMe only costs $15 and equally they do not provide you with any specific health recommendations or interpretations.  But they do add a filter which makes it easier to identify the genes on the OMIM website.  OMIM is part of the the US National Library of Medicine and it is an invaluable tool. 

However, there is a catch. 23andMe and livewello (or any of the other gene apps) only identify SNPs and do not adequately look at copy variances and deletions. Still there is useful information, which in knowledgeable hands can give helpful information.

In the near future, (like after Autism One and IMFAR) I will write up an interpretation guide for the primary genes I find helpful and with that I hope to further all of our understanding of the emerging field of personal genomics.  Remember – knowledge is power – what you do with that power can change your life in important ways through the use of informed choices. 

Clinical Trial on the Use of a Unique Form of Transcranial Magnetic Stimulation – MRT for the Treatment of Autism is Nearing Completion – Results to be Presented at Autism One 2014 in Chicago.

Clinical trial NCT01985308 (details available at or directly at is in its final stages of completion.  The preliminary results of the study will be presented during the Autism One conference upcoming in Chicago in May ( ). MRT uses powerful magnetic pulses to stimulate the brain is unique ways.  The outcomes from the early use of MRTwere recently presented by Prof. Yi Jin, the developer of this type of therapy at the annual AANS meeting.


I’ve had the pleasure of working the Brain Treatment Center team including various technicians Prof Jin and his sister Dr. Toni JIn for the past several months on this project. The study has been arduous and Toni has put in some amazingly long hours to help the parents, the children and me with this complex area of research.

The study recruited 28 subjects with autism ages 4-12 and entered them into a 12 week program.  The treatment required frequent EEG testing and examinations. The magnetic (MRT) portion was based on the EEG findings and uniquely tailored for each patient by the assessments of individuals neurophysics (electronic signature of the brain).  The study had/has two arms with each group being randomly assigned to either 5 weeks of sham and then 5 weeks of treatment and the other group getting 10 continuous weeks of treatment. Everyone remained blinded and the seal on the numerical codes will not be broken until the end of the study.

I hope you join Drs Jin and myself at Autism One for a look at the use of MRT for autism.  For more information about MRT you may visit and if this is something you feel may apply to your child you may contact my office for a consultation.  MRT, a form of TMS, is only available by prescription and requires the supervision of a physician. The FDA has approved TMS for the treatment of refractory depression. It is not approved for the treatment of other disorders including autism and its use is considered an off-label application of the technology which is permitted in the US. Additional research is expected to start in the next 12 months at UCSD regarding its use in autism.

International Interest in Stem Cell Therapies for Autism Continues to Grow Amidst Ongoing Controversies

I am pleased to announce today’s publication in the World Journal of Stem Cells of our review of Mesenchymal Stem Cells (MSCs) for the treatment of autism.  Our team representing Italy, the US and Ukraine, reviewed the evidence and present understandings of this important class of stem cells and what we know about its potential and rationale for autism therapeutics. We also discuss various struggles, including regulatory restrictions in various countries, for the present application of the MSCs to autism treatment. Here in the US I routinely extract adipose derived stems cells (mostly MSCs) for the treatment of arthritis – primarily knee joint degenerative disease. This is a relatively simple application of stem cell therapeutics and I am about to publish our initial outcomes from this.  I DO NOT HOWEVER TREAT AUTISM WITH STEM CELLS HERE IN THE US. I use EmCell in Ukraine for advanced autism related cell interventions.  Together with the EmCell team, I have submitted our outcomes in the autism population for publication and it should be available soon in print. If after reading this article – via the link below – you are interested in stem cell therapies, you may contact my office to set a time for consultation.


The Link to the Public and Freely available article is here:

The Autism Nexus: New Discovery of a Link Between the Gut Microbiome, the Immune System, Brain Dysfunction and Vitamin D and Vitamin D Binding Protein (GcMAF)

I am very proud of our recent work published in the highly regarded Journal of Inflammation.  By clicking on the hyperlink you browser should take you straight to the article which is available for no cost at the journal’s website. Once you are there click on the pdf button (the yellow arrow shows you where to click once you get to the article on the web).  Before you jump to article page let me explain in easier language why this article is so important. It is the first article any of us as authors have written that was accepted without any critique or changes, which means the reviewers thought very highly of it. While that is important, it is only part of the significance of our findings.  It has always bothered me that minor changes on the gut bacteria and yeast (microbiome) could result in wild and crazy changes in a child’s behaviors. While that observation is common among those of us treating the biology of autism, it was actually very difficult to understand mechanistically at the level of the child’s biology, at least until now.

We believe we have uncovered the nexus (intersection) of the observations regarding Vitamin D deficiency, GcMAF observed improvements in behavior, see: , immune dysregulation, brain inflammatory changes (mostly in microglial regulation), and the microbiome.  Briefly, the endocannabinoid system is part of the cell systems that regulate the immune system and the brain. In particular, it seems the CB2R (cannabinoid 2 receptor) reads the background environment of the individual (diet, microbiome, etc) and sets the tone of the immune defenses.  Last year we published the first observations of CB2 dysfunction in autism (J Autism Dev Disord. 2013 Nov;43(11):2686-95. doi: 10.1007/s10803-013-1824-9.). With this follow on work it seems likely that the endocannabinoid system is at the center of the complex biomedical disruptions underpinning the autism epidemic we are observing.  Now for your homework. Go the Journal of Neuroinflammation website and get the entire article. After you read it you can ask you questions. (use the link provided in the first paragraph).


JNI Article facepage

CDC data show continued rise in autism spectrum prevalence for Autism Awareness month



You can download the entire article and go over the statistics for yourself but here are a few of the outstanding observations these data offer us.

1) The ADDM site prevalence has risen to 2.38% of boys and 0.5% of girls, although in figure 4 of the report it goes as high as 2.75% of boys.

2) The median age of diagnosis of autism was 53 months (4 years 5 months).

3) The disorder is diagnosed more frequently in the white non-Hispanic population




You won’t be able to read this chart on your mobile phone very easily, but the data are certainly terrible for our children.

As a background in statistics, 10 case per 1000 in prevalence equals 1%, so the prevalence for both boys and girls combined in the sum of the ADDM areas was: White non-Hispanic 1.58%, Black 1.23%, Asian 1.23%, Hispanic 1.08%.  The overall ratio of boys to girls was 4.76 to 1.

Based on the available scientific literature it is difficult to explain the nearly 5 fold increased risk of ASD observed in the make population. The simplistic observation would be to look at the Y (male) and X (female) chromosomes and see what is happening there.  Very few autism risk factor genes have been identified on either chromosome apart from fragile X which accounts for only a small percentage of ASD cases. This implies some epigenetic (gene-environment) interaction wherein males show more vulnerability than the females. Finding these factors has been elusive, but a new study may give us some clues.


The American Journal of Human Genetics. 94, 415–425, March 6, 2014

This is a complex study, but the apparent observation is that females have significantly higher numbers of small copy-number variants (CNVs) in the DNA (more mutations) but have less risk of autism – meaning being female somehow lends protection to the gene variations and implies males are more sensitive to genetic variations.  As with previous studies these factors are NOT occurring on the sex chromosomes, but rather on the other chromosomes.  They also observed higher levels of neurodevelopmental risk factor genes in the mothers compared to the fathers of the children with ASD, which was again consistent with the view that females tolerate a higher burden of CNVs than males.


The odds ratio of having a neurodevelopmental associated gene CNV was 3 times higher for females than males (15% compared to 5%). However, only 308 of 4482 males (6.87%) tested in this study actually had CNVs detected.  So even this study fails to explain on a genetic basis the genetic risks of autism for the majority of cases.

This leaves us still searching for the combination of genes and environmental factors triggering this incredible and frightening rise in ASD observed in the most recent CDC study. I will be presenting more on this at Autism One in Chicago this year.

Autism Says Goodbye to 2013 and Hello to 2014: Breakthroughs and Progress

As it ended, 2013 turned out much better than I expected. I received a special present on Christmas Eve when, Itai Berger, Editor of Frontiers in Human Neuroscience, emailed me that my article on transcranial ultrasonography had been accepted and was available online in provisional format.  See abstract below.

Frontiers Abstract

This publication was the result of ongoing collaborations with my Italian colleagues at the University of Firenze (Florence). Professors Ruggiero and Pacini are pushing the immunological research in autism, chronic fatigue syndrome (ME/CFS), and cancer through their detailed laboratory investigations of the vitamin D binding protein – GcMAF. It was our shared interest in GcMAF that brought us together on the ultrasound research.  2012 ended with the publication of the first article describing Nagalase and GcMAF in ASD. (title below).


One year later – to the day and after more than 10,000 article views – I was lecturing in Dubai at the 2nd International Conference on GcMAF Immunology.  The conference was well attended with physicians and researchers fro many countries. Pediatricians and Psychiatrists from Dubai, Jordan, Turkey, Italy, India and the US shared their experiences with GcMAF therapy in ASD.  It was very rewarding to hear their stories. They presented videos and collections of cases, all of which observed something similar to what i had already published: most children with autism respond vigorously to GcMAF and side-effects were minor and transient.

gcmaf conf dubai

I consult with families from 37 different countries around the globe and I hear the same stories about GcMAF regardless of the child’s ethnicity or culture. That likely speaks to the immunological ties between immune dysfunction and autism.  Below is one of the many extraordinary letters I received late in 2013.

Once upon a time my first born son was autistic.

       He stopped developing properly around the age of 1 and lost the few words and skills he previously had, though I don’t believe he was up to par even then. From there he slipped away from us into his own world and it was as if he couldn’t even see or hear us. He didn’t know he had a name, that we had names, or that we were even there. He didn’t babble, he didn’t play with toys, he didn’t even look up at people when they entered the room. When we had kids over to play he would hide in a corner and cry. He was chronically ill with one sickness after another, always tired, sleeping 14 hours at night and if we woke him up from his nap before 3 hours he would scream hysterically sometimes for 2 hours. The first doctor told me he was just a boy and boys develop slower, the second doc said we were just bad parents, and the third finally gave us a diagnosis at 27 months – 8 months after I had begun to worry.

     We tried everything; B-12 shots, ABA 20 hrs. a week, speech, OT, vitamin D, probiotics, and an extremely strict diet of no gluten, dairy, eggs, nuts, soy, fish, dyes, preservatives or anything artificial. These things did help a lot but even so it was an extremely difficult uphill battle of working months to gain a skill and if one person wasn’t consistent on the implantation of a goal he would regress immediately. There was a whole year that he woke up screaming every night for hours. Nothing I did helped and he couldn’t tell me what was wrong so I would resort to laying beside him and crying myself. He would wake up his baby brother who then also began screaming. It was a long year of screaming even from me! I once responded to one of his fits by having an all out screaming meltdown of my own, face down on the floor pounding the ground like a 2 year old. I was depressed, exhausted, and contemplated many times just ending it all…I have to be real because other parents need to know they are not alone in this. Besides the screaming he was always horribly constipated to the point of needing medical intervention, he had raging eczema head to toe, was allergic to literally everything; I knew my son was sick. I often told my husband, “some day 50 years from now the doctors will finally figure out that autism is a problem with the immune system but by then it will be too late for him.” I thought he would live with us his whole life and just continue to be a tired, sick, crying, itchy boy, who couldn’t get words out or look at us. Then my friend told me she found a doctor named Bradstreet who did believe it was immune related and was treating it! I had hope!          

     We started GCMAF and began seeing real progress after the level 7 dose. He seemed more energetic, cried less, and speech and eye contact were improving. Each week began to be amazingly better than the last and it felt like we were seeing actual recovery. Then after about a month he ended up in the hospital with a raging sinus infection of strep that led to an abscess behind his eye. This is a very rare complication but as I said, he had the immune system of a flea. He needed emergency surgery to save his eye but continued to battle the infection and a fever of 104 for 11 days until they resorted to surgery again, this time fully removing his right ethmoid sinus.  During his hospital stay and for 3 weeks after while he was still on antibiotics we couldn’t do GCMAF. His regression was significant. His speech went way back to about 9 months before we started GCMAF, he could only get a few words out at a time with great difficulty and even I couldn’t tell what he meant. He actually said to me finally, “mommy. help me,” and I said, “with what baby?” He struggled to get out the following, “with the…words…not come….out… good.” I cried because I knew he felt trapped in his own body unable to do what he was trying to. When I told him the shots were going to help him be able to speak he was eager to get them and reminded me every week on Wednesdays.

     When we started back up again and finally got the progress going he developed a rash which I now know was molluscum but at the time thought it could be related to GCMAF. We changed his dose from the level 12 once a week to level 5 twice a week and then we lost him. He went off into “autism-land” as I call it. Didn’t hear us, couldn’t focus, couldn’t even accomplish a single step direction and wandered around aimlessly. This dosage was working for other kids but not for him. We went back to level 12’s once a week and after 6 weeks of that he was in everyone’s mind effectively cured.

     His speech and OT discharged him, and after 2 weeks of being in a typical kindergarten class with no aid, the school coordinator told me he didn’t even need any special accommodations. We increased his school day to be full day now from 8:30-3:30 and even though he isn’t even 5 yet, there are zero problems. Zero. No fits, no meltdowns, no non-compliance. His teacher told me he listens in class, follows the schedule with no extra prompting, plays with kids on the playground, holds his pencil properly (big one!), and even sits with friends asking them where they live and what they ate for snack. After school he is able to tell me what he did, describe details about movies or books they read, sing me songs he learned, and he still has energy to play and doesn’t melt down when we get home. He never previously had the skills of recalling events or asking/answering questions properly until this. He currently has no therapy and we see no autism in him whatsoever. He says what he wants when he wants fluently, uses slang terms and laughs at jokes! He has even developed a little bratty back-sass attitude which my husband and I correct but then turn to each other and cry happy tears because it’s SO normal!! He was actually able to tell me that he likes the shots because his sleep is better, he has more energy, and he can speak better. He also hasn’t gotten sick once since the hospital stay back in March. His bowels are no longer dependent on laxatives daily as they were for 2 years. It’s like a dark cloud has been lifted and my son has been freed from his internal prison. We have the son we never had but knew was in there somewhere dying to get out. I have no doubt he will live a normal life and accomplish anything he wants to from now on. I don’t know if he will need GCMAF permanently or not but even if he does I don’t care. I will never let him go back into that cave. I firmly believe God answered my prayers and healed my son and he used Dr. Bradstreet and GCMAF to do it. Our son is healed and so is our family.

Forever indebted and grateful beyond measure,

His Mom

As a parent (and I am one with 2 boys, my own son and my step-son are both on the autism spectrum) these stories are powerful and touching.  But as a scientist I am driven to understand the mechanisms behind these types of anecdotes. The story relates a child rapidly changing state from significant and non-verbal autism, to observed to be normal by parents, teachers and therapist over a mere few weeks.  Autism has been felt to be a developmental and irreversible brain disorder. Clearly that is not always the case, as many stories of recovery are being published in the lay literature.

So how can this happen?  Mechanistically, I think this must represent the presence of an interfering inhibitor to normal neurological functioning. Whatever this substance or effect is, it acts very much like local anesthesia blocking signals in specific parts of the brain. In at least the example described above, that effect is then rapidly dissipated and the brain essentially wakes up. This story is common and doctors at the conference in Dubai presented their own versions describing very similar events in their practices as well. But not all children respond to GcMAF and that speaks to various subtypes of the disorder, some of which are readily recovered while others seem much more entrenched in whatever autism represents at the brain level.

It appears a significant subset of autism is immunological driven and that would fit the observations noted from around the world regarding GcMAF as a therapy. The graphic below is from a review article: Gesundheit B, Rosenzweig JP, Naor D, Lerer B, Zachor DA, Procházka V, Melamed M, Kristt DA, Steinberg A, Shulman C, Hwang P, Koren G, Walfisch A, Passweg JR, Snowden JA, Tamouza R, Leboyer M, Farge-Bancel D, Ashwood P. Immunological and autoimmune considerations of Autism Spectrum Disorders. J Autoimmun. 2013 Aug;44:1-7. doi: 10.1016/j.jaut.2013.05.005. Epub 2013 Jul 15.


IN the graphic the authors depict the maternal immune system with its macrophages and other immune cells priming the response of microglial cells in the fetus.  Microglial cells are derived from macrophages which migrate into the brain during fetal development.  Those macrophages then undergo changes to become microglial cells.  They, however, maintain many of the features of their original macrophage immunochemistry. Missing from the diagram is another intersect circle representing the postnatal environmental effects. But regardless of that limitation in the representation, the hypothesis they propose is chronic immune – inflammatory changes in the brain secondary to microglial swelling.

GcMAF as noted in my paper, stands for Gc protein macrophage activating factor.  That name makes it sound like a pro-inflammatory molecule and as such based on the model above it would seem to be the last thing you would want to give to a child with autism.  As it turns out, the argument for chronic inflammation in the brain of children with autism is not universally agreed upon and other researchers, particularly Prof Manuel Casanova, have the opinion there is no inflammation in the autism brain.

I had the pleasure of sitting with Prof Casanova at several autism-related think tanks where the immune system was being discussed.  He took a decidedly differing view that there was no evidence of inflammation in the autism brain, but rather there was abnormal construction of the brain’s special electronics and at its smallest unit the minicolumn.  Casanova explained he had dissected scores of brains in great detail and inflammation was not present.  Instead the consistent finding was abnormal minicolumn construction. Below is an excerpt from a complex but insightful review we must consider.


How is it that both camps: the inflammatory and the minicolumn, can be so divided in their views of autism?  First, I agree that autism is primarily influenced by epigenetic factors. In 2013 I participated in a review of these factors which is public access.


In this review we wrote: “The term epigenetics was first coined in the 1940s by British embryologist and geneticist Conrad Waddington, who described it as: “the interactions of genes with their environment, which bring the phenotype into being” [17]. Our present knowledge enhances this earlier understanding, and epigenetics now evaluates the alteration of DNA transcription via variations in DNA methylation and histone modifications, but without alterations in the DNA sequence. These variants represent the epigenome, which in turn will be reflected in the transcriptome: that portion of the DNA which is being actively transcribed into RNA.”  The key is the environment regulates DNA transcription (messaging) without changing the sequence (no mutations) of the DNA.

Let’s return to the original article I posted on Transcranial Ultrasonography of the Brain.  An important part of that research was the publication of this research in Brain:image

And most importantly this observation; that there was too much fluid around the brain of children with autism.



In the figure above I excerpted the images from Shen, et al., 2013 and added the arrows and notations of increased EAF.

In our paper on TUS we observed the same effect – increased fluid surrounding the brain. Below is a side-by-side comparison of fraternal twins from our paper in Frontiers in Human Neuroscience (2014).


Under normal conditions the fluid (hydrostatic) pressure of the subarachnoid space (the fluid surrounding the brain) is not sufficient to keep the space fully open at the point where the brain folds itself closely to the skull.  In figure 13 from our paper, you can see the space of Twin A stays constant at 0.16 cm as the underlying brain compresses the arachnoid (meninges) of the brain, whereas with Twin B the space is compressed down to 0.01 cm. Now go back to the images from the Brain study of Shen, et al., 2013. If you study those images you will see that in the neurotypical child, the gyral summits (places where the brain folds up towards the overlying inside of the skull) come is very close proximity to the inner lining of the meninges and typically seem to be touching the membrane.  In our higher magnification views we see the same effect (Twin B). However, we and Shen, et al., 2013 observe the same increased distance of fluid volume in the case of autism.

So what does this mean?  At a recent MAPS conference I pulled Professor Theoharides aside to discuss my observations.  “Theo”, as well al call him, is a brilliant Mast Cell researcher and you can pull up his publications at his website:  I will insert a portion of one article, but realize Theo has extensively published on the immune and mast cell effects in ASD.


The graphic below is in my opinion a more complete understanding of the immune and epigenetic effects than the one from Geshundheit, et al., 2013.


This graphic gets us closer to what I think is really happening in autism, but it leaves out the potential role of the very much neglected meninges in the development of autism. Theo agreed this was an intriguing notion and one of my projects is to finish a review of this factor with Theo in early 2014. What I now theorize happens in autism is somewhat like happens in experimental models of multiple sclerosis – although obviously different in timing and specificity.




The meninges make the EAF which fills the subarachnoid space – that same EAF and subarachnoid space which is observed to be increased both both us, Bradstreet, et al., (2104), and Shen, et al., (2013).  In the research above, the inflammatory changes in the subarachnoid space, what both Shen, et al., 2013 and we think is is happening, induce changes in the microglial cells of the cortex making them more appear more inflammatory and less ramified (supportive).


The cells are noted to be round and this is the way they look when they are inflammed.

In direct distinction, GcMAF treated microglial cells convert to the supportive ramified state. This means that the effect of GcMAF on microglial cells and macrophages is NOT inflammatory, but the opposite – anti-inflammatory.

In findings soon to be published, the images dramatic support this effect. I believe the shifting of macrophages and glial cells to anti-inflammatory states can explain why and how the mother’s story of her son’s recovery happened. To more fully understand this we need to understand the birectional role of TNF-alpha on memory and brain development.

TNF-alpha is one of the most potent pro-inflammatory mediators of the immune system.  At proper concentrations it is required for development of memory and synaptogenesis.  At pathological levels it destroys synaptic communication and is part of all neurodegnerative disease states including Alzheimer’s. New evidence points to the effects of TNF-alpha on NMDA receptor function.




In my clinical practice, I use MgThreonate routinely and it is nearly always helpful in autism. The mechanisms are speculative but it is both effective at NMDA-R restoration as noted above as well as a direct anti-inflammatory.

Tying these seemingly unrelated observations together gets me to where I think autism is taking our understanding.

1). Epigenetic, both prenatal and postnatal effects influence the priming of microglial cells and most assuredly mast cells as well.

2). Mast cells and macrophages contribute to inflammatory changes in the meninges.

3). The immune changes in the meninges opens the tight junctions in the capillaries and allows extra fluid to accumulate in the subarachnoid space.

4). The increased EAF also carries within it the inflammatory chemistry of the mast cells and macrophages.

5). This message also influences the microglial cells and the mast cells resident in the brain.

6). This disrupts minicolumn function and structure.

7). This process prevents the creation of proper harmonic communication in the electrical properties of the brain.

8). The end result is autistic symptoms.

Presumably GcMAF and Magnesium threonate work to restore both microglial cells and macrophages to the ramified supportive non-inflammatory state.  The effect of mast cells in unknown.  But with all of this I believe 2014 is going to bring some amazing breakthroughs for relieving the suffering of autism.

So Happy New Year – 2014


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