Flux Health Forum

Autism, GABA and the Brain Gauge

Short summary: The Brain Gauge methods predicted GABA deficits in autism that were later validated with medical imaging.

After having many discussions with lots of people who are interested in the Brain Gauge technology, I became increasingly aware that a vast majority assume that the Brain Gauge was designed and is only used for assessing traumatic brain injury (TBI) or concussion and nothing else. Although we have received support from the Office of Naval Research for the development of the Brain Gauge as a standardized concussion tool, we actually started the development of the device as a means for studying alterations in brain health, and the first funded projects that we were awarded for were in the field of Autism research. The US Army sponsored one of our first projects, and this funded our efforts for building the precursor to the Brain Gauge (the first one weighed in at over 15 lbs even though it was the world’s first portable tactile stimulator!).
Some of my previous research had to do with the investigation of minicolumns – the smallest functional unit in the cortex – and how the organizational scheme created by minicolumnar structure impacted information processing in the cortex. There was a good bit of research on that particular topic in the autism field, as a scientist named Manuel Casanova (you can see his website here https://corticalchauvinism.com/ ) had discovered significant differences in the organization of minicolumns in individuals with autism. His studies utilized post-mortem histology, and he showed that there were 30% more minicolumns in individuals with autism than people without autism. A sample of his work is pictured below:


These are histological sections (stained for cell bodies) of controls on the left and autism on the right. Note the higher density of the vertical arrays of cells on the right side. This finding led us to design some sensory tasks to demonstrate that sensory percept would be altered in autism. To summarize, we found that the test results were consistent with the idea (1) that individuals with autism were functionally impacted by the higher density of minicolumns in a positive manner and (2) that interactions between minicolumns were significantly altered in a negative or developmentally disabled manner. It was speculated that this increased density of minicolumns came at a cost – that is, because the cells were so tightly packed (and in a less organized manner) the connections between the minicolumns were disrupted. In particular, the inhibitory connections, or those mediated by GABA (the primary inhibitory neurotransmitter in the cortex), were impacted.
One thing that we found in our initial study was that plasticity of the individual with autism was significantly impacted and this was consistent with the idea that GABA deficits could play a significant role in the disorder.
In order to standardize the testing a bit better, we developed some new tasks that focused on the subject’s ability to adapt to a stimulus. Adaptation is very sensitive to GABA deficits and your ability to adapt to a stimulus is synonymous with plasticity (you can read more about that here: https://insights.corticalmetrics.com/plasticity-measure/ ).

We found some significant differences between our control subjects and our autism subjects. To summarize, this is a summary bar chart of what we found with adults with autism:


Since our initial study, many other researchers have adopted the Brain Gauge methods for studying autism and in particular, adolescents with autism. The plasticity deficit has been consistently found and reported in other studies and that measure has also been correlated with GABA deficits with MRS imaging (you can read that Puts et al 2016 study here: https://downloads.corticalmetrics.com/pub/puts_reduced_2016.pdf )

What that correlation means is that there is less GABA in the individual with autism, and that the less there is, the lower their plasticity score is.

The feedforward inhibition metric in autism is also well below normal (more details on this in a later post), and this hints that not only is there an inhibitory deficit due to low GABA, but that it is probably a GABAb deficit (two types of GABA in the brain: GABAa and GABAb; another article will detail this, but if you want to read about it in the scientific paper you can do so in Favorov et al 2017 ). There are currently no methods for differentiating GABAa vs. GABAb in the living human cortex, although this information could be very significant for guiding treatment. We believe that this highlights the importance of these types of methods that you can perform with the Brain Gauge and we will continue to pursue this line of research with our collaborators.

Interested in reading more? The Brain Gauge has taken part in quite a few autism studies and if you would like to read them, you can find them by going to www.corticalmetrics.com/publications and typing “autism” in the search bar.

I was reading about the minicolumns and Manuel Casanova was talking about it as a shower curtain of inhibition and was using TMS successfully with autistic patients.

So, somehow I have to internally make a chain between the concepts of GABA, the Brain Gage as being able to measure something useful and eventually get to TMS as having a positive effect.

I have a young man who has been diagnosed back and forth between Autism and other psych things and it has frustrated the mother so much that every time the professionals change, the diagnosis changes.

I can’t convince you to have a beer and make a science music video for me? Laughing, I love science music videos and science animation and anything funny better than PubMed.

I have been thinking about autism. I have always had a little bit of shyness and self-consciousness and after my brain was injured it became more like a social anxiety and my friend’s young son who has autism has similar characteristics.

The day before yesterday, I used the M-1 to see if I could calm down and get over shyness and self-consciousness. I visualized having my ACC tell my pre-frontal cortex to calm down, which they say doesn’t happen in autism and it definitely hasn’t been happening for me for the past 6 years. But I always was self-conscious. The brain issues just magnified it considerably. I have been separating myself from everybody because of not wanting to offend people and I know that I need plasticity in those areas, not to avoid interaction.

Well, today, I was left alone at work and had social interaction and it went well. Then, tonight, I had a sweet Jewish woman accidentally dial my phone number looking for Talbots and she and I spoke for probably 2 hours and it was so easy for me to interact and I didn’t have even one self-conscious second. Not one. No fear at all. I also still don’t have fear about the event which I am going to this weekend.

I only did one session for this and combined it with binaural beats and practicing mindfulness.

I still have ZERO social anxiety and spoke for 2 hours to a total stranger. She was sweet and my buy an ICES, who knows. She has pain.

When my foot and ankle were injured, I couldn’t walk properly for years and was in pain and had one leg swell up twice the size of the other leg and I used the ICES for one day and the swelling went down and I was able to walk and haven’t had pain since. One session.

Same thing for sleep. One session and I slept after a decade of insomnia.

I am not sleeping tonight because I spoke on the phone all night long and didn’t get my work done, but when I use the ICES, I sleep on demand and I stopped being frustrated and afraid of trying to sleep and making it worse. I can sleep without it. Though without it, I fall asleep around 2, but for over a decade, I didn’t fall asleep until after 4, often after 5 and when I tried to fix it, after 7.

If I healed my social anxiety and it doesn’t come back, I won’t even know what to do.

I still don’t know if I had a stroke, but if I did, it wasn’t like Bob’s stroke. I didn’t go to the doctor and I didn’t do therapy. I started falling and hitting my head and may have had a stroke, then, got concussions, then, lost most of my relationships and definitely got Diabetes and didn’t treat it and I feel like God is helping me and I know that Bob already said not to mention that topic on his video, but he could be wrong about that one topic. Maybe.

I am wondering if social anxiety might be related to something like inflammation or if it is related to something like too little gamma (like Alzheimer’s) or some other mechanism.

For each case, one session changed everything. For my back and shoulder, it didn’t work that way, but for those things, it did. There has to be a mechanism.

For my foot and ankle, inflammation seems like the right answer.

I know that depression is strongly linked to inflammation, but is social anxiety? Is sleep?

There are things like renewing my brain in the area of food, which seriously took a while, but I expected social anxiety to take longer than that. I didn’t expect to not be dreading the weekend already.


Cognitive recovery has been slow even with the ICES.

It seems like maybe things related to inflammation get healed in a single session and other things take time.

My foot and ankle pain went away in one day. My back pain and shoulder pain went away, but it was not nearly as impressive.

@Mark Are there any areas where you might suggest experimentation using the ICES PEMF coils to increase GABA? I would like to use my ICES M1 and my Brain Gauge to self experiment on this.

@Mark @Bob Any suggestions on using ICES PEMF to increase GABA/ improve Brain Gauge performance with those relevant metrics?

We really do not have any information on ICES and GABA. That is something I would love to know, but for now it is squarely in the realm of self-experimentation.

Hi @Bob, any thoughts on where to start with the self-experimentation beyond gut health and vagus nerve stimulation? Thanks as always for any insight you can share!

That’s the challenge. Just figuring out how to measure the thing you want to know, how to do the experiment itself, that’s the first and most important problem. Just measuring the biological effects of PEMF is nearly impossible. We just do not have reliable biomarkers.

This is the key problem with all of medical science. This is why it takes so long, so many decades of study, just to begin to start to hope to try to do any meaningful biomedical experiment where you can actually measure (and heaven forbid, prove, anything).

You could spend many lifetimes just studying this one very challenging aspect of biomedical research.

There are hundreds, really millions of examples of what we do not know how to measure in biomedical research. As just one example, did you know that until we developed the brain gauge, there was absolutely no way to measure mild brain injury or concussion. None. (people lie about this, but that is the truth)

And what we think we know how to measure… just try it some time. Go ahead. I double dog dare you. Try to actually measure the change in your GABA levels when you apply PEMF. And even if you can do that, how do you know the finding can be generalized to other people?

So, where to begin? I honestly don’t know, but if you figure it out, please, by all means, let me know.

Yep, I get it. I will report back if I discover any personal nuggets worth sharing.

GABA increases, Brain Gauge and test result/parameters…

I have GABA self generation problems as shown in a section of my Neural Zoomer test panels. It is the assessment of my Functional Neurologist that the Purkinje cells in my cerebellum are not properly functioning at a healthy level. Chronic neural inflammation is also contributing factors as well due to 55years of PTSD, numerous repetitive TBI impacts, several different strains of herpes virus etc.

My objective is to influence this deficiency upward to help calm me down and reduce my impulsive outbursts with an added objective of reducing my chronic insomnia.

I supplement with liposomal GABA, a transdermal GABA cream and also take GABA Complex products which help the body promote a relaxed consciousness. I am not immediately focused on optimal dose level, rather than results. These efforts are currently underway and also include the following use of ICES devices.

A very friendly frequency for the cerebellum is in the Aplha range and for this application I will use the mu setting. In addition to the controller I match it up with the quad coil configuration held over the lower skull and at the top of the spinal column on the backside of neck and skull intersection with a headband.

I usually also employ a CES 0.1 micro amp square wave at 10 hertz onto my Auricular Branch Vagus Nerve.

My objective is to increase blood flow in the cerebellum area and hopefully encourage my cerebellum to regain some plasticity resulting in a natural increase in GABA production.

When a highly left brained developed individual is lacking in GABA production it is a very noticeable calming effect when you can actually get some GABA past the blood brain barrier. And yes I am feeling some personal improvements in the goal areas previously described.

But as Bob has stated, my approach is so inclusive that there is no way to determine how much relief I am getting as per measured GABA increases in my body. However it bears repeating that I am getting positive results in that my hair triggered anxiety level is WAY down and I actually find myself relaxing and thinking through angry trigger events rather than automatically and instantaneously attacking perceived threats.

Yes, impossible to design a test for but this is working for me so I will lab to continue. Bob’s device and quad coil are so easy to wear with either a headband, bandana, or cap to keep the coil in place.

I hope this encourages us to try different approaches and combinations of therapies to use with the ICES/PEMF devices.

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0.1 amp for current rating not 0.1micro amp in the above posting

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Another correction for OP.

OK, too much coffee OR not enough?

The setting is actually on TENS stimulation not CES.

Boy what a messy posting this morning! I apologize to anyone whoe reads it

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Hi…I also have issues specific to low GABA!

Mine arose after a recurring virus (something like EBV)

are you finding any protocols specifically helpful to you, I see you mention using the ICES tech but I’m having a hard time understanding what protocols you’re actually using. I have a C5 and an A9. It’s very useful simply for chronic pain but the advanced, experimental programs on the C5 tempt me…there’s so many. Maybe I’ll just do as Bob says and test the programs out, carefully, low power at first etc, and maintain some sort of record of what I feel so I can kind of reflect on what the different programs seem to do. I’m always looking for a quicker answer on this stuff lol.

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10hz across the lower rear of skull attempting to affect the cerebellum and encourage damaged Purkinje cells to produce more GABA.

Plus trans dermal and liposomal GABA supplements do help a lot!

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