Join us for a live Q&A session on mental health and neurofeedback featuring an incredible panel of experts! ποΈ This session will tackle your most pressing questions on brain health, trauma recovery, neurofeedback, and more. π§ Panelists Include: Jay Gunkelman: Neurofeedback legend with over 500,000 brain scans analyzed. Dr. Mari Swingle: Author of i-Minds and a leader in neuroscience and psychology. Joy Lunt: Expert in neurofeedback for autism, sensory processing disorders, and more. Joshua Moore: Renowned neurofeedback practitioner and educator. John Mekrut: Advocate for neurofeedback in PTSD and mental health. Dr. Andrew Hill: Brain health expert and founder of Peak Brain Institute. Santiago Brand: International leader in biofeedback and neurofeedback. Anthony Ramos: Neurofeedback practitioner and mental health advocate. Pete Jansons: Host of the NeuroNoodle Podcast. π When: Tomorrow, October 2nd at 6 PM CST πΊ Where: Live on YouTube β Donβt miss it! Get your questions ready for a dynamic discussion on how neurofeedback can improve mental health, brain performance, and overall well-being. We'll also dive into the latest research and practical tips for brain optimization. π Subscribe and hit the notification bell to stay updated and join us live! #Neurofeedback #MentalHealth #BrainHealth #QandA #JayGunkelman #DrMariSwingle #JoshuaMoore #JohnMekrut #AndrewHill #SantiagoBrand #AnthonyRamos #JoyLunt #NeuroNoodle #LiveStream #BrainPerformance #TraumaRecovery
Episode Summary
I joined the NeuroNoodle panel with Jay Gunkelman, Dr. Mari Swingle, and a roomful of practitioners to take audience questions on neurofeedback, brain health, and the things people get wrong about both. This conversation originally aired on NeuroNoodle; you can watch the original conversation. What follows are my own observations from that discussion, with the science laid out the way I think about it from the research and the brain maps.
How fast does neurofeedback actually change the brain?
People ask me whether brain training is slow. Compared to a pill, yes. Compared to how the brain normally changes, it is remarkably fast.
Here is the scale I care about. With neurofeedback the research describes moving people meaningfully against population norms over a few months. That is a large shift for human transformation. I get jaded about it, and I catch myself thinking "oh, this person only had a little change in their ADHD, and it took six weeks." Six weeks is nothing. For the person living inside that brain, it is life-transformative.
I spent years around traditional acute mental health care before this. What I saw there was palliative care, suffering, and revolving doors. People suffer for decades. Then you train a circuit and the research and the brain maps show the slowing lift in a matter of months. Fourteen years of reading maps in, it still feels like cheating.
Months is fast for the brain. It is astonishingly fast for the person. If you want a fuller picture of what the evidence supports, I cover it in Is Neurofeedback Legitimate? A Research Overview.
Can neurofeedback improve comprehension and memory?
Yes, with a caveat about what training can and cannot do.
Semantic and declarative memory are tied to alpha frequency tuning. When alpha is tuned appropriately, recall tends to improve (Klimesch, 1999). The limit is real: you can tune for memory, but you cannot create a memory of something you never learned. The information has to be encoded first. Training the brain improves the capacity to receive, process, interpret, and reproduce information. It does not replace studying.
SMR Neurofeedback: Train Sleep, Focus, and Self-Control is one of the relevant tools here. There was a nice study out of Salzburg, Austria on SMR training and the visual event-related potential. The SMR work cleared a somatosensory interference that was contaminating the visual ERP (Kropotov et al., 2005). It stabilized the brain and cut out the cross-talk. SMR training also supports semantic and declarative memory consolidation and sleep (Hoedlmoser et al., 2008).
The honest framing: SMR has a learning curve. Think of it as a slow-release upgrade to your existing equipment. If you want the deeper dive on memory mechanics, I wrote Biohacking Memory: Optimizing Encoding, Consolidation, and Retrieval.
Why stimulants help some ADHD brains
Methylphenidate (Ritalin) reduces frontocentral theta. In a large slice of the ADHD population that slow frontocentral activity is associated with reduced dopamine signaling linked to dopamine transporter genetics. The dopamine transporter strips dopamine away from the striatum, so you have a leak. Methylphenidate is a dopamine reuptake inhibitor; it plugs the leak, and you end up with an appropriate amount of dopamine. Good match for that phenotype. Neurofeedback gets at the same frontocentral slowing through training rather than pharmacology. I go through this in Does Neurofeedback Work for ADHD? A Neuroscientist's Guide.
Should you be chasing more neuroplasticity?
The biohacking world has this backward. Unchecked plasticity is a liability. People are microdosing and stacking compounds to crank up plasticity, and that is the wrong target. Shape the plasticity you have. If you want more, meditate.
Open the plasticity window without a shaping signal and you are just rolling the dice on what consolidates. People get into trouble with psychedelics and with non-psychedelics for exactly this reason.
Neurofeedback is a potentiator. It sets the brain up for many other things. That is a feature worth respecting, because it also means the changes keep coming. I have watched microdosers stop microdosing and effectively start macrodosing without realizing it, because brain training amplified what they were doing. Exercising your brain makes all kinds of things stronger, including effects you did not intend.
For the disciplined version of plasticity, read Biohacking Plasticity: Unlock Your Brain's Adaptive Potential, and for shaping it through practice, Mindfulness: Don't Just Do Something, Sit There.
Can neurofeedback remyelinate white matter?
Probably, but there are more reliable primary approaches to remyelination.
CDP-choline (citicoline) has research behind it for membrane and myelin support. Hyperbaric medicine and possibly photobiomodulation offer plausible metabolic support, and dietary inputs matter too. Those approaches may help the cells you are training with neurofeedback grow. I would not reach for neurofeedback as the primary remyelination tool.
That said, the published findings are striking. Work from Robert Coben's group used pre-post connectivity and imaging measures in autism, and the neurofeedback appeared to track with changes in the areas being trained (Coben & Padolsky, 2007). The neurofeedback appeared to sculpt white matter in the areas being trained.
The mechanism connects to what we see in the spectra. In significant autistic presentations you find Delta in the temporal areas, and that Delta is associated with white matter that developed atypically. At the developmental level where myelin gets laid down, the tissue can be over- or under-myelinated. Over-myelinate and you effectively turn a neuron off. Under-myelinate and it is not a high-speed neuron. Either way it does not work right. Left temporal slow content tracks with language problems; right side tracks with the Asperger's-type presentation. When training drops that slow content, the imaging shows the white matter in the area resolving toward normal.
I would not have expected white matter to be neurofeedback-responsive. The fact that it has been observed is the point. When the Delta drops, the alpha frequency tunes up, the beta spindling clears, and the function in that region climbs. The neurological turf gets ready, and then the occupational therapy, the speech and language work, all the other interventions start landing. The brain becomes available to accept the input.
Gamma is sneaky: why you should be cautious training it
Gamma is the band where careers get damaged by overclaiming. Persistent gamma is associated with pathology. You see it in seizure foci, in dystonias, in chronic pain, in parkinsonism. A vendor once asked me to write something favorable about gamma-training software, and I told him that if I write about gamma, I also write about the pathology. Persistent, tonic gamma is something you want to understand before you touch it.
Nested gamma is a different animal. Gamma is an emergent property of a network. When a network forms, gamma rings about 45 milliseconds afterward, the way a bell rings. It is a resonant property of the network, not a state you tonically elevate. You see it nested in chirps of theta, and in sensory areas you see it nested in alpha. Using wavelets, you can watch event-related synchronization and desynchronization, roughly six bursts of gamma per second. In high-functioning ADHD those bursts are weak. In lower-functioning ADHD the nests are often empty. Gamma in ADHD is under-evaluated and undertreated, and it matters.
A practical warning to anyone newer to this: bringing gamma up helps in certain narrow conditions and does real harm in others. Get the literature solid and find a mentor before you touch it.
Can you measure gamma with passive electrodes?
You can, with caveats. The argument against passive electrodes comes down to the one-over-f problem. Delta sits at high amplitude; as you climb in frequency the amplitude drops for the same energy. All that EEG passes through layers of tissue and gets attenuated. Gamma frequently sits below the noise floor in low-end equipment.
Measuring gamma with non-active electrodes requires a clean environment, high electrode density, and analysis beyond simple FFTs. With a $500 amp and passive electrodes, you are not getting that resolution. Many early EEG gamma findings were confounded by electromyographic artifact (Whitham et al., 2007; Yuval-Greenberg et al., 2008). A Hilbert transform, which looks for synchronicity rather than power, surfaces real gamma far more readily than an averaged data set.
There is also the gamma-versus-gamma-2 distinction. The 40 Hz gamma everyone talks about is one resonant function. Higher-frequency resonances, gamma-2 ripples, are sometimes deeply involved in pathology. Look at someone in an acute schizophrenic break who is hearing command voices in that moment. You will see beta spindling and excess power up in the 30-something Hertz range. That is pathology sitting in the range people loosely call gamma.
The Davidson monk research that everyone cites is not the gamma we usually mean. That work, with Cliff Saron and others, involves gamma synchrony ringing far above the usual band, not tonic high-amplitude gamma (Lutz et al., 2004). Different phenomenon, different claims.
Why do practitioners avoid training the frontal poles directly?
The frontal pole sites (Fp1, Fp2) are noisy. They sit right on top of muscle and the field of eye movement, so the signal is contaminated. They are hard to train cleanly, and they produce delayed effects. The research and the maps show second-day or third-day effects from FP sites, which means if you are running several sessions a week you can overshoot where you wanted to go before the effect even shows up.
Moving slightly up to AFz, FPz, or FZ picks up enough of the anterior cingulate without the artifact. With a 19-electrode QEEG you usually have adequate source localization to find where the problem originates and place an electrode that feeds it back. Orbitofrontal work for trauma is done commonly; you simply do not need to drive the sensor into the worst part of the field. For what a full map shows, see QEEG Brain Mapping: What It Is, What It Shows, and What to Expect.
My own bias is to work corticothalamically. I am thalamus-first in how I think about protocols. I try to find the central manipulation that regulates broadly before I go hunting for individual patches of cortex to tune. People are also strongly connected to their somatosensory cortex; the felt sense of central feedback is strong, which makes that training more intuitive for them than work in regions our language barely describes.
The autism, gut, and insula connection
A large share of autism cases show GI problems, and that is no surprise once you look at the insula (McElhanon et al., 2014). A substantial proportion also show epileptiform activity, and the insula is easily a focus.
Walk down the homunculus from feet to hands to face, dip into the Sylvian fissure, and the posterior insula governs gastrointestinal motility through smooth muscle regulation. A discharge there produces a smooth-muscle spasm in the intestines rather than a striated-muscle seizure, and that spasm is painful. Abdominal epilepsy is recognized in the literature, though it remains uncommon and outside the international classification system.
In one published case, a young patient's aura was an internal distress sensation. Her seizure started in the left insula, spread, and showed up with high voltage on the right temporal lobe, which surgeons were prepared to remove. The actual trigger was the left insula. Neurofeedback targeting the focus stopped her seizures. She has been seizure-free for over seven years.
Before anyone leaps to the brain, rule out the simple things. Constipation is often a somatic expression of anxiety. Magnesium deficiency is common and responds to supplementation. Try the simplest solution first, then escalate. If GI specialists scope a patient and find nothing, that is when looking at the head becomes reasonable. Abdominal migraine likely shares a top-down vagal mechanism with these presentations, and migraine and epilepsy share comorbidity in the literature, with some migraine patients responding well to anticonvulsants like topiramate.
What lead and other toxins do to the developing brain
Leaded gasoline almost certainly contributed to learning problems across several decades. Lead gets stored long term in bone, and it is very hard to remove. Mercury is similar, and how deeply it lodges depends on its form; methylated mercury is absorbed deep. Different toxins store in different compartments, fat or bone.
This is a public health failure. Refineries vent hydrocarbons and heavy metals; one Bay Area facility settled after years of releases, with metals showing up in dust across the community. Many chemicals banned in Europe remain on US shelves. The damage from early lead exposure is largely fixed, which is why prevention matters more than any after-the-fact training protocol.
The bottom line from the panel
Neurofeedback tunes circuits, clears interference, and prepares the brain to absorb other therapies. It works on a timescale of months, which is fast for tissue and transformative for a person. It is a potentiator, which means the changes keep compounding, and that demands respect for what you pair it with.
If you are considering it, start with a proper QEEG to see what your brain is actually doing, then build a protocol around the findings. Read Biohacking with EEG Phenotypes: Predict Your Brain Function to understand how your individual pattern shapes the plan, and consult your physician before changing anything in your care.
References
- Klimesch (1999). EEG alpha and theta oscillations reflect cognitive and memory performance: a review and analysis. doi:10.1016/s0165-0173(98)00056-3
- Kropotov (2005). ERPs correlates of EEG relative beta training in ADHD children. doi:10.1016/j.ijpsycho.2004.05.011
- Coben (2007). Assessment-guided neurofeedback for autistic spectrum disorder. doi:10.1300/j184v11n01_02
- Lutz (2004). Long-term meditators self-induce high-amplitude gamma synchrony during mental practice. doi:10.1073/pnas.0407401101