Robert Hedaya
Georgetown University School of Medicine
Robert Hedaya is a psychiatrist whose work focuses on the intersection of biology, brain function, and mental health. His published research covers clinical applications of quantitative electroencephalography (qEEG), qEEG-guided laser therapy, dual-AI systems for medical error detection, and nutritional and herbal interventions for pain.
22 claims checked on air: 1 context 1 contradicted 1 overstated 12 supported 7 unverified
What they said on air - supported
1 citing their own research
Panic attacks involve activation of adrenaline in the brain and locus coeruleus triggering.
"And panic is basically separation anxiety where you think you're going to die, and then deep parts of the brain—you trigger the adrenaline in the brain, the locus coeruleus gets activated, and you're like, "I'm going to die," and you have panic." (said at 0:09:11)
The speaker's statement accurately reflects standard neurobiological models of panic attacks and panic disorder. The locus coeruleus is the primary noradrenergic nucleus in the brainstem, and its activation—along with hyperactivation of central noradrenergic pathways (often referred to colloquially as brain adrenaline)—is a central component of the neural circuitry and fear networks mediating panic responses.
- supports: Noradrenergic function in panic disorder. (The Journal of clinical psychiatry 1990)
"Pharmacologic or electrical activation of noradrenergic neurons of the major brain noradrenergic nucleus, the locus ceruleus (LC), has anxiogenic effects in nonhuman primates. Elevated LC neuron firing is associated with anxiety or fear responses in freely moving cats. These observations are supported by clinical investigations that have demonstrated abnormal noradrenergic system regulation in panic disorder patients." (abstract, results, passage verified)
pubmed - supports: Functional neuroanatomy in panic disorder: Status quo of the research. (World journal of psychiatry 2017) · cited 100x in the literature
"Gorman et al (1989; 2000) proposed a comprehensive neuroanatomical model of PD, which suggested that fear- and anxiety-related responses are mediated by a so-called "fear network" which is centered in the amygdala and includes the hippocampus, thalamus, hypothalamus, periaqueductal gray region, locus coeruleus and other brainstem sites... Advanced neurochemical studies have substantiated the major role of serotonergic, noradrenergic and glutamatergic neurotransmission in the pathophysiology of PD." (abstract, introduction and results, passage verified)
pubmedfull study (doi)
Red blood cell MCV reference range is typically 80 to 100 fL, and elevations can indicate B12 deficiency.
"The size of her red blood cells, the MCV, the mean—it was one, not really high. It was 101, the range 80 to 100. I ignored it because two reasons... I looked it up and it says, "Oh, could be a B12 deficiency. Do a Schilling test."" (said at 0:10:15)
The standard reference interval for mean corpuscular volume (MCV) in adults is 80 to 100 fL. An MCV above 100 fL defines macrocytosis, and vitamin B12 deficiency is one of the most common recognized causes of elevated MCV.
In depression, quantitative EEG demonstrates impaired interhemispheric communication and reduced information flow between the left and right frontal lobes.
"So in depression, for example, you'll see that the frontal lobes are not talking to each other. The information is not flowing from left to right and right to left, right?" (said at 0:21:07)
Quantitative electroencephalography (qEEG) studies examining functional connectivity and coherence in patients with major depressive disorder frequently demonstrate reduced frontal interhemispheric coherence and disrupted communication between the left and right frontal regions compared to healthy controls. Reviews of the literature identify decreased frontal interhemispheric EEG coherence as one of the most consistent neurophysiological markers associated with depressive disorders. Because these findings are derived from cross-sectional and observational neurophysiological studies with variability across frequency bands and clinical sub-types, the overall certainty is low.
Mycoplasma infections can localize to and affect the basal ganglia.
"Mycoplasma goes to the basal ganglia, for example, I've seen it. And then you treat the Mycoplasma, and you actually see the QEEG change over time." (said at 0:23:11)
Published clinical and neuroimaging literature confirms that Mycoplasma pneumoniae infection can involve and damage the basal ganglia, most often presenting as parainfectious or post-infectious basal ganglia encephalitis, bilateral striatal necrosis, or associated movement disorders. Systematic reviews and case series document neuroimaging showing lesions localized predominantly to the basal ganglia or cerebellum, commonly thought to be mediated by autoimmune mechanisms (such as antineuronal/antiganglioside antibodies) or direct central nervous system complications.
Streptococcal infections in children can trigger pediatric autoimmune neuropsychiatric disorders (PANDAS) affecting the basal ganglia and caudate nucleus, causing OCD symptoms.
"We know PANDAS, you know, strep infection with some kids goes into OCD in the basal ganglia and the caudate nucleus, etc." (said at 0:23:39)
The claim accurately reflects the prevailing medical understanding and working pathophysiological hypothesis for Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS). Clinical diagnostic criteria established by Swedo et al. define PANDAS as a post-streptococcal autoimmune condition characterized by abrupt-onset obsessive-compulsive disorder (OCD) and/or tics (PMID: 15241433). Multiple imaging and functional studies demonstrate neuroinflammatory changes and microstructural alterations localized to the basal ganglia, specifically the caudate nucleus and putamen (PMID: 25117419, PMID: 32364596). Autoantibodies from children with PANDAS target neuronal antigens in the basal ganglia and specifically bind to striatal cholinergic interneurons, altering their function (PMID: 32670106, PMID: 32539528).
- supports: PANDAS: current status and directions for research. (Molecular psychiatry 2004) · cited 203x in the literature
"The working hypothesis for the pathophysiology begins with a GAS infection in a susceptible host that incites the production of antibodies to GAS that crossreact with the cellular components of the basal ganglia, particularly in the caudate nucleus and putamen. The obsessions, compulsions, tics, and other neuropsychiatric symptoms seen in these children are postulated to arise from an interaction of these antibodies with neurons of the basal ganglia." (abstract, conclusions, passage verified)
pubmedfull study (doi) - supports: Evaluation of basal ganglia and thalamic inflammation in children with pediatric autoimmun… (Journal of child neurology 2015) · cited 163x in the literature
"Binding potential values, suggesting underlying activated microglia-mediated neuroinflammation, were found to be increased in bilateral caudate and bilateral lentiform nucleus in the PANDAS group and in bilateral caudate nuclei only in the Tourette syndrome group, compared to control group." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Antibodies From Children With PANDAS Bind Specifically to Striatal Cholinergic Interneuron… (The American journal of psychiatry 2021) · cited 100x in the literature
"Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections, or PANDAS, describes such a situation after infection with Streptococcus pyogenes ... IgG from children with PANDAS bound to CINs, but not to several other neuron types, more than IgG from control subjects, in three independent cohorts of patients." (abstract, background and results)
pubmedfull study (doi)
Laser therapy applied to the brain increases cellular ATP production.
"And I'm like, "Oh my god, this could really help the brain. This is amazing cuz it's giving ATP. It's doing a lot of different things we could talk about, but I was blown away."" (said at 0:26:44)
Transcranial photobiomodulation (PBM) or low-level laser therapy (LLLT) uses red to near-infrared light absorbed by mitochondrial cytochrome c oxidase (complex IV). This stimulation enhances mitochondrial respiration and cellular adenosine triphosphate (ATP) synthesis. In vivo animal models and human neuroimaging studies using phosphorus-31 magnetic resonance spectroscopy (31P MRS) have demonstrated that transcranial light delivery increases cerebral ATP synthase flux and tissue energy metabolism.
Approximately 2.6% to 4.2% of transcranial laser light penetrates through into the brain.
"the laser penetrates about 2.6% of the light gets through that we know. Some people say 4.2%, about 2.6% let's say." (said at 0:32:24)
Published experimental and computational studies examining near-infrared (NIR) light penetration through human head tissues (scalp and skull) indicate that light transmission to the cortical surface generally ranges from 0.2% to 10%, depending on the wavelength (e.g., 808–810 nm), beam power, skull thickness, and anatomical site. The stated figures of approximately 2.6% to 4.2% fall squarely within this established scientific range.
Photons from transcranial laser therapy dissociate nitric oxide from mitochondrial complexes, thereby boosting ATP production and increasing blood flow.
"the photon from the light actually knocks off a nitric oxide molecule and then the ATP flows through. It's more complicated than that, but the ATP now instantly flows through. Now, you have more energy... Then you have the nitric oxide bringing more blood flow." (said at 0:35:00)
The speaker accurately describes the established primary mechanism of action for red and near-infrared photobiomodulation (low-level light/laser therapy). Cytochrome c oxidase (Complex IV of the mitochondrial respiratory chain) serves as a primary photoacceptor. Absorption of light in the red to near-infrared spectrum photodissociates inhibitory nitric oxide (NO) from the enzyme's catalytic center. This displacement relieves metabolic inhibition, restores electron transport and proton-motive force to increase ATP synthesis, while the liberated nitric oxide acts as a vasodilator to increase local blood flow.
- supports: Proposed Mechanisms of Photobiomodulation or Low-Level Light Therapy. (IEEE journal of selected topics in quantum electronics : a publication of the IEEE Lasers and Electro-optics Society 2016) · cited 1612x in the literature
"One of the most important chromophores is cytochrome c oxidase (unit IV in the mitochondrial respiratory chain), which contains both heme and copper centers and absorbs light into the near-infra-red region. The leading hypothesis is that the photons dissociate inhibitory nitric oxide from the enzyme, leading to an increase in electron transport, mitochondrial membrane potential and ATP production." (abstract, passage verified)
pubmedfull study (doi) - supports: Transcranial Photobiomodulation to Improve Cognition in Gulf War Illness. (Frontiers in neurology 2020) · cited 25x in the literature
"Red/NIR wavelengths are absorbed by cytochrome C oxidase in mitochondria, releasing nitric oxide (increasing local vasodilation), and increasing adenosine tri-phosphate production." (abstract, introduction, passage verified)
pubmedfull study (doi) - supports: Molecular Mechanisms of Photobiomodulation in Retinal Diseases: Cytochrome c Oxidase, Mito… (International journal of molecular sciences 2026)
"At the molecular level, PBM acts primarily through photon absorption by cytochrome c oxidase (CcO, complex IV of the mitochondrial electron transport chain)... Photon capture promotes photodissociation of inhibitory nitric oxide (NO) from the binuclear CuB-heme a 3 centre, accelerates electron transfer, restores the proton-motive force and increases ATP synthesis." (abstract)
pubmedfull study (doi)
Photobiomodulation reduces and reverses misfolding and accumulation of alpha-synuclein, tau protein, and beta-amyloid in neurodegenerative disease models.
"misfolded proteins, you know, proteins in the brain that don't fold right and they cause problems and they're like they're like viruses. They spread, right? And it actually reduces that and reverses alpha-synuclein folding in a dementia protein... And tau protein, you know, all these things, beta-amyloid" (said at 0:35:45)
Preclinical research in animal models of Alzheimer's and Parkinson's disease demonstrates that photobiomodulation (near-infrared light therapy) can attenuate the accumulation and pathology of beta-amyloid plaques, tau hyperphosphorylation, and alpha-synuclein toxicity. For example, long-term transcranial photobiomodulation in transgenic Alzheimer's disease rodent models significantly reduced amyloid plaque burden and tau hyperphosphorylation while enhancing microglial clearance and mitochondrial function. Similarly, photobiomodulation mitigated neurotoxicity and neuronal loss in rat models of alpha-synuclein overexpression. Because these findings are derived from preclinical animal and cell culture models, certainty in human clinical application remains very low.
Dr. Robert Hedaya published the first case report of cured acquired prosopagnosia treated with laser therapy.
"So I published it. It was the first ever cured acquired prosopagnosia, facial blindness." (said at 0:39:48)
Dr. Robert Hedaya published a 2022 single-patient case report detailing the reversal of acquired associative-type prosopagnosia following quantitative electroencephalography-guided transcranial laser therapy (qGLT), with no recurrence noted at 1-year follow-up. Because this evidence comes from a single uncontrolled case report, the therapeutic efficacy of this intervention carries very low certainty and requires further controlled study.
Variations in glucocorticoid-pathway genes including NR3C1, FKBP5, and CRHR1 impair cortisol receptor signaling and increase vulnerability to PTSD and depression.
"A big one is genetic glucocorticoid resistance. So um steroid corticosteroids, which we make, those are stress hormones, right? So there are a set of genes, uh five genes: NR3C1, FKBP5, CR receptor 1 and 2, CR-binding... because the cortisol doesn't hit the receptor properly. It doesn't translate to the genes to tell the genes that you're under stress... Now you have PTSD much more easily, right?" (said at 0:56:15)
Genetic variations in hypothalamic-pituitary-adrenal (HPA) axis and glucocorticoid-pathway genes—notably NR3C1 (encoding the glucocorticoid receptor), FKBP5 (a co-chaperone regulating glucocorticoid receptor sensitivity), and CRHR1 (corticotropin-releasing hormone receptor 1)—are significantly associated with altered glucocorticoid receptor signaling and vulnerability to posttraumatic stress disorder (PTSD). Meta-analyses and systematic reviews confirm that specific single nucleotide polymorphisms and gene-level variations in FKBP5, NR3C1, and CRHR1 modulate stress-response pathways and increase the risk of developing PTSD, particularly in interaction with trauma exposure.
- supports: Genetics of glucocorticoid regulation and posttraumatic stress disorder--What do we know? (Neuroscience and biobehavioral reviews 2016) · cited 85x in the literature
"Glucocorticoid action is regulated by a corticotrophin-releasing hormone, arginine vasopressin (AVP)/oxytocin pathway, GR, and regulators such as co-chaperone FKBP5. Single nucleotide polymorphisms (SNPs) in the GR gene, CRHR1 gene and FKBP5 gene affect HPA-axis sensitivity. The GR gene SNP BclI has been associated with hypersensitivity to glucocorticoids and PTSD symptoms. FKBP5 gene SNPs interacted with childhood adversity to moderate PTSD risk and in particular, the rs9470080 SNP was independently associated with lifetime PTSD. SNPs in the CRHR1 gene were also associated with PTSD risk." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Meta-Analysis of Associations Between Hypothalamic-Pituitary-Adrenal Axis Genes and Risk o… (Journal of traumatic stress 2020) · cited 38x in the literature
"Findings from SNP-level analyses indicated that two variants (rs9296158 in FKBP5 and rs258747 in NR3C1) were nominally associated with PTSD, ps = .001 and .001, respectively, following multiple testing correction. At the gene level, significant relations between PTSD and both NR3C1 and FKBP5 were detected and robust to sensitivity analyses. Although study limitations exist (e.g., varied outcomes, inability to test moderators), taken together, these results provide support for FKBP5 and NR3C1 in risk for PTSD." (abstract, results, passage verified)
pubmedfull study (doi)
Linus Pauling won Nobel Prizes for his work related to protein structure and for his peace advocacy on the Nuclear Test-Ban Treaty.
"he won the Nobel Prize for for folding of proteins, but also um for the Peace Prize for the Nuclear Test-Ban Treaty in the '60s." (said at 1:04:08)
Linus Pauling received two unshared Nobel Prizes matching the speaker's description: the 1954 Nobel Prize in Chemistry for his research into the nature of the chemical bond and its application to complex structures (notably including the discovery of protein secondary structure elements like the alpha-helix and beta-sheet) and the 1962 Nobel Peace Prize (awarded in 1963) for his peace advocacy and campaign against nuclear weapons testing, which was instrumental in leading to the 1963 Partial Nuclear Test Ban Treaty.
- supports: Linus Carl Pauling, 28 February 1901 - 19 August 1994 (Biographical Memoirs of Fellows of the Royal Society 1996) · cited 9x in the literature
"He is best known, perhaps, for his insights into chemical bonding, for the discovery of the principal elements of protein secondary structure, the alpha-helix and the beta-sheet, and for the first identification of a molecular disease, sickle-cell anaemia, but there are a multitude of other important contributions... For these achievements, Pauling was awarded the 1954 Nobel Prize in Chemistry... His active opposition to nuclear testing brought him political persecution in his own country but was finally influential in bringing about the 1963 international treaty banning atmospheric tests. With the award of the 1962 Nobel Prize for Peace, Pauling became the first person to win two unshared Nobel Prizes" (abstract, passage verified)
openalexfull study (doi)
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