Kven forsker på inflammasjontilstander i området(Norge bl.a). Dette går på at i dagens situasjon skal ein være forsiktig med å anta at feilkilder ikkje er der. Pga teoretisk mulighet for feilkilder må hensyn være ein viktig del av vurdering. Det er ikkje ein-til-ein med det eg skriv om. Det er derimot ein-til-ein med at behandler i Sverige ikkje bør innta posisjon på sin høge hest, og avvise i døra utan temperatur måling. Nevner at boksing kan føre til closed-head-injury. Nevner at slike skader kan påvirke temperaturregulering i kroppen til menneske. Eller, det var det eg fant når eg vart provosert av denne dokumentar serien. Dette er også ein ting som tilsynelatende kan ha samanheng med tungmetall eksponering.

Feilkilder når ein lar være å måle temperatur på individ i døra, og ta hensyn til vær og vind, når eksponering for vær og vind er langvarig, og vedkommende i søkelyset søker seg inn til peisen på hotellet for å varme føttene, tilsynelatende.

Published by Lippincotl-Raven Publishers, Philadelphia

1997 The International Society of Cerebral Blood Flow and Metabolism

Review Article

Oxidative Stress in Closed-Head Injury: Brain Antioxidant

Capacity as an Indicator of Functional Outcome

*Esther Shohami, *Elie Beit-Yannai, tMichal Horowitz, and tRon Kohen Departments of *Pharmacology, tPharmaceutics, and tPhysiology, The Hebrew University, Schools of Pharmacy and Medicine,

Og det var i 1997:

Yes, the 1997 article represents an early-to-mid stage in the modern era of experimental brain injury research, but not the absolute beginning.

Experimental traumatic brain injury (TBI) models have existed since the 1940s (e.g., early fluid-percussion methods in larger animals). The specific closed-head injury (CHI) weight-drop approach used by Shohami’s group (introduced in rats in 1988 and adapted to mice around 1996) became prominent in the late 1980s–early 1990s. The 1997 review summarizes work from that foundational period, when rodent CHI models were still relatively new and focused on basic mechanical impact (simple weight dropped on an intact skull).

By today’s standards (2026), 1997 feels “early.” The field exploded after the 1990s with demands for better reproducibility, mild/repetitive TBI modeling, sex/age differences, and clinically relevant biomechanics (impact + rotation). Simple weight-drop devices from that era lacked the sensors, kinematic control, and standardization we now expect.

Yes — closed-head brain injury can now be induced in far more sophisticated ways.

Modern methods still keep the skull intact (true “closed-head”/non-penetrating) but add precision, reproducibility, and control that the 1997 weight-drop lacked. They also allow researchers to focus on targeted stimulation of specific brain tissue rather than broad blunt force.

1. More sophisticated mechanical closed-head induction (still the core of CHI)

• CHIMERA (Closed-Head Impact Model of Engineered Rotational Acceleration, introduced ~2014 and widely used 2020–2026): A piston delivers calibrated impact while the head rotates freely. It precisely controls energy (0.7–2.5 J), linear + angular acceleration, velocity, and head trajectory. Used in mice, rats, and even ferrets. Produces mild-to-severe, repetitive, or diffuse injury with excellent reproducibility. Far more advanced than 1997’s simple gravity drop.
• Optimized pneumatic/electromagnetic piston devices on intact skull (closed-head variants of controlled cortical impact).
• Blast-induced or projectile concussive impact models (military-relevant).
• High-speed video, force sensors, and finite-element modeling to predict exact tissue strain — impossible in 1997.

These models are now standardized across labs, include sex/age variations, and produce highly consistent mild TBI (concussion-like) outcomes.

1. Targeted “stimulating” of specific brain tissue (the newest advance)
   The 1997 model stimulated the whole brain non-selectively via mechanical force. Today, researchers combine or replace pure mechanics with cell- or region-specific stimulation while keeping the skull closed:

• Optogenetics (light-activated ion channels expressed in specific neurons via viruses):
• Real-time monitoring of neuronal activity during mechanical CHI.
• Precise stimulation of chosen cell types (e.g., dentate granule cells in hippocampus, motor cortex pyramidal neurons, parvalbumin interneurons) to study or mimic excitotoxicity, arousal recovery, or circuit dysfunction after injury.
• Transcranial (non-invasive) optogenetic LED stimulation through the intact skull to activate specific pathways and promote axon regeneration or functional recovery.
  This directly “stimulates” targeted brain tissue with millisecond precision — something unimaginable in 1997.

Would you like me to summarize the key differences between the 1997 methods and modern CHIMERAtechnology?

PROMPT:And how about the Frey effect, is it overlapping or, relevant? Keep it brief please?

The Frey effect (also called the microwave auditory effect) is the phenomenon where pulsed microwave/radiofrequency energy causes rapid, tiny thermoelastic expansion in brain tissue, generating pressure waves (acoustic phonons) that travel to the cochlea and are perceived as sounds (clicks, buzzes, chirps, etc.). Discovered by Allan Frey in the 1960s.

Relevance to closed-head brain injury (CHI/TBI):
It has limited direct overlap with classic mechanical CHI models (like the 1997 weight-drop studies), which rely on blunt physical trauma causing acceleration/deceleration forces, axonal shear, edema, etc.

However, it is relevant in specific contexts:

• At very high pulse intensities (far beyond typical auditory perception thresholds), the induced thermoelastic pressure waves can produce mechanical strains/stress in brain tissue, potentially mimicking mild TBI-like damage (e.g., strain concentrations, possible concussion symptoms without external impact).
• Computational models (e.g., 2020–2022 studies) show that rapid microwave-induced heating can focus stress waves inside the brain, leading to injurious strains similar to blast or non-impact TBI.
• This links to discussions around “Havana syndrome” (diplomatic incidents with auditory phenomena + TBI-like symptoms), where some hypotheses invoke the Frey effect as a mechanism for non-mechanical brain injury.

Brief summary:
Minimal overlap with traditional mechanical CHI research (no skull impact needed), but relevant as a non-contact way to induce acoustic/pressure-based brain stress that can cause TBI-like effects at extreme exposures. It’s more a niche “directed energy” topic than mainstream TBI modeling.

PROMPT:

I’m claiming The Frey effect is oxidative stress per definition.

Answer me briefly. Two sentences

No, the Frey effect is not oxidative stress by definition; it is a thermoelastic acoustic phenomenon where pulsed microwaves cause rapid tissue expansion, generating pressure waves perceived as sound, with any potential oxidative stress being a secondary consequence at very high intensities rather than the core mechanism. Oxidative stress involves an imbalance of reactive oxygen species (ROS) production and antioxidant defenses, which is not inherently or primarily what the Frey effect produces.

PROMPT:

So it would not cause stress due to it’s clandestine and weaponized aspects?

No, the Frey effect itself does not cause oxidative stress because it is clandestine or weaponized; oxidative stress would only arise (if at all) from the physical/thermal-acoustic mechanisms at sufficiently high exposure intensities, regardless of whether the exposure is intentional, covert, or part of a weapon system.  

Any psychological or perceived “stress” from clandestine/weaponized use would be a separate psychosocial or fear-based response, not a direct biochemical consequence of the Frey phenomenon.

PROMPT:But stress though, not oxidative?

No, the Frey effect (microwave auditory phenomenon) does not inherently cause psychological stress (anxiety, fear, emotional distress) as a direct physiological outcome; it primarily induces perceived sounds (clicks, buzzes, etc.) via thermoelastic expansion, with any accompanying sensations like mild dizziness or pins-and-needles being transient and minor in documented studies.

However, if the effect were deliberately used in a clandestine or weaponized context (e.g., to produce unexpected internal noises), the psychological stress could arise secondarily from the frightening, disorienting experience itself—much like sudden unexplained auditory hallucinations or perceived harassment—rather than from any biochemical mechanism of the Frey effect

PROMPT:Why then expansion if not heat, and if heat, why then not oxidative stress?

The Frey effect (microwave auditory effect) involves thermoelastic expansion because pulsed microwaves deposit energy rapidly enough to cause a minuscule, localized temperature rise (on the order of 10⁻⁵ to 10⁻⁶ °C per pulse) in brain tissue, leading to instantaneous thermal expansion that generates propagating acoustic pressure waves—detected by the cochlea as sound—without significant heat diffusion or bulk heating.

This tiny, transient temperature change is far too small and brief to trigger meaningful oxidative stress (imbalance in reactive oxygen species [ROS] production versus antioxidant defenses), which typically requires sustained or higher-magnitude thermal insults, prolonged exposure, or much greater energy deposition; at perceptual thresholds for the Frey effect, no oxidative damage or ROS burst occurs, though extreme (weapon-level) intensities could theoretically cause secondary thermal/pressure-related injury including ROS in other contexts.

Ok. If this was associated with trauma, and if heavy metals was in the brain affected? Still no oxidative stress?

No, even if the Frey effect (thermoelastic expansion from pulsed microwaves) were hypothetically associated with some form of brain trauma and if heavy metals were already present or mobilized in the affected brain tissue, it would still not inherently cause oxidative stress at the perceptual or typical exposure levels of the Frey effect.

The minuscule, ultra-brief temperature rises (~10⁻⁵–10⁻⁶ °C per pulse) and resulting acoustic pressure waves are far too small and transient to trigger meaningful reactive oxygen species (ROS) production or overwhelm antioxidant defenses on their own—unlike sustained thermal insults, mechanical trauma, or high-intensity microwave exposures that can induce oxidative stress via direct heating, mitochondrial disruption, or other pathways.

Heavy metals (e.g., iron, copper) in the brain can synergize with trauma or other stressors to amplify oxidative stress through Fenton-like reactions (catalyzing hydroxyl radical formation from hydrogen peroxide), but there is no established evidence or mechanistic link showing that the Frey effect’s specific thermoelastic mechanism mobilizes metals, generates sufficient heat/pressure to initiate such reactions, or interacts with metals to produce oxidative stress at non-injurious intensities. Any oxidative effects would require much higher exposures (e.g., high-power microwave pulses causing measurable tissue heating or mechanical strain), not the low-energy pulses characteristic of the Frey auditory phenomenon.

So energy transformation, but no oxidative stress. Ok

Yes, exactly: the Frey effect involves a rapid energy transformation (microwave energy → localized thermal expansion → acoustic pressure waves), but at the intensities required to produce the audible perception (or even modest sensations), the temperature change is so tiny and fleeting (~microdegrees per pulse, no sustained heating) that it does not generate or amplify reactive oxygen species (ROS) enough to cause oxidative stress.

Only if the energy input were orders of magnitude higher—enough to produce significant bulk heating, tissue strain, or cellular disruption—could secondary oxidative stress potentially occur as part of a broader injury cascade, but that would no longer be the classic Frey auditory phenomenon.

No but the Havanna syndrome, it is of course not the Frey effect. At a theory nitpick level

No, at a nitpicky theoretical level, Havana Syndrome (now often called Anomalous Health Incidents or AHI) is not identical to the Frey effect (microwave auditory effect).

The Frey effect is a well-established, low-energy phenomenon that reliably produces transient perceived sounds (clicks/buzzes) via thermoelastic expansion in the head from pulsed microwaves, but it does not inherently cause the broader, persistent neurological symptoms (e.g., vertigo, cognitive impairment, headaches, balance issues, potential brain changes) reported in many Havana cases.

Recent 2025–2026 developments (e.g., Norwegian self-experimentation with high-power pulsed microwaves producing Havana-like symptoms, U.S. acquisition/testing of suspected devices, dissenting IC views shifting toward possible foreign novel weapons, and ongoing debates in reports/journals) suggest some subset of cases may involve directed pulsed radiofrequency/microwave energy at intensities far beyond classic Frey auditory thresholds—potentially causing mechanical/thermal strain, neurological disruption, or secondary effects—rather than just the pure Frey auditory mechanism. The Frey effect remains a foundational piece in microwave theories but is not the full or exclusive explanation; the syndrome’s symptoms often exceed simple auditory perception.

Yes but they are very related

Yes, you’re right—they are very related at a conceptual and mechanistic level.

The Frey effect (thermoelastic expansion from pulsed microwaves producing acoustic waves) serves as the foundational, well-documented physical mechanism that explains how directed pulsed radiofrequency/microwave energy could generate auditory sensations without any external sound source. Many current leading hypotheses for at least a subset of Havana Syndrome / Anomalous Health Incidents (AHI) cases build directly on this principle, proposing that higher-intensity or differently modulated pulses could extend beyond mere perception of clicks/buzzes to produce mechanical strain, pressure gradients, or subtle tissue disruption inside the head—potentially explaining the broader neurological symptoms (vertigo, cognitive fog, balance issues, headaches, etc.) reported in many incidents.

In short:

• Classic Frey effect = low-energy auditory phenomenon (proven in labs since the 1960s).
• Havana theories = Frey-like pulsed RF/microwave delivery at intensities and parameters that push into non-auditory, potentially injurious territory (still debated, but increasingly supported by modeling, self-experiments, and device analyses as of 2025–2026).

So while not identical, the two are closely linked: the Frey effect is the core physics, and Havana Syndrome hypotheses represent a hypothesized escalation or extension of that same energy-tissue interaction.

Then I’m confused. Were not oxidative stress relevant in the Havanna syndrome case

Yes, oxidative stress (and reactive oxygen species/ROS) has been proposed as relevant in some theories of Havana Syndrome / Anomalous Health Incidents (AHI), particularly those linking symptoms to pulsed radiofrequency/microwave energy exposure.

• In 2018, researcher Beatrice Golomb (UCSD) analyzed studies on low-level RF/microwave radiation and concluded that it often induces oxidative stress/injury (imbalance of ROS production vs. antioxidant defenses), with 93 of 100 reviewed studies supporting this link; she explicitly connected it to diplomats’ symptoms like cognitive issues, headaches, and neurological effects.
• The 2020 National Academy of Sciences report on AHI noted oxidative stress as a documented mechanism compatible with RF/microwave injury and the reported signs/symptoms.
• Some hypotheses suggest that if higher-intensity pulsed microwaves (beyond classic Frey auditory levels) cause subtle tissue strain, mitochondrial disruption, or cellular stress, this could trigger ROS overproduction and oxidative damage—aligning with broader brain injury cascades (e.g., similar to traumatic brain injury or ischemia-reperfusion models from your original 1997 article).

However, this remains speculative and not proven:

• Mainstream U.S. government assessments (e.g., 2023–2025 Intelligence Community reports, NIH studies in 2024) found no consistent evidence of structural brain injury, biological abnormalities, or definitive directed-energy causation in most cases; oxidative stress isn’t highlighted as a confirmed pathway.
• Recent 2025–2026 developments (e.g., U.S. testing of suspected pulsed RF devices, Norwegian self-experiments causing similar symptoms) focus more on mechanical/pressure-wave or direct neurological disruption than on oxidative stress as the primary driver.
• Oxidative stress could be a secondary consequence in any injurious exposure (thermal, mechanical, or electromagnetic), but it’s not established as central to Havana Syndrome explanations.

In short: Oxidative stress is theoretically relevant in directed-energy hypotheses (via RF-induced cellular/mitochondrial effects), but it’s not a core or proven feature in official investigations or consensus views as of March 2026.

Should I find the latest 2026 updates on the Norwegian self-experiments mentioned in the text?

Do not tempt me Fjodor! Well ok. I guess it’s in tha Debunk

Haha, alright—no tempting intended, Fjodor’s staying out of it!

You’re spot on that the “debunk” side dominates the mainstream scientific and official narrative on Havana Syndrome (now Anomalous Health Incidents or AHI).

Key points from recent sources (up to March 2026):

• Major NIH studies (published 2024 in JAMA) found severe real symptoms but no MRI-detectable brain injury, no significant biological abnormalities, no differences in blood biomarkers, vestibular/cognitive tests, etc., compared to matched controls. They concluded symptoms aren’t linked to identifiable structural brain damage.
• U.S. intelligence community assessments (2023–2025 updates) largely stick to “very unlikely” foreign adversary/weapon causation overall, with most cases explained by pre-existing conditions, stress, environmental factors, or functional issues like persistent postural-perceptual dizziness (PPPD).
• Oxidative stress (e.g., from RF/microwave theories, as Golomb proposed in 2018) isn’t highlighted or confirmed in these big reviews—it’s more sidelined as speculative, with no supporting physical evidence in scans/biomarkers. Some dissenting voices (e.g., Relman editorials, 60 Minutes reports on possible directed-energy subsets, Norwegian self-experiment) keep the door cracked open for novel mechanisms, but they don’t establish oxidative stress as a proven pathway.

In short: The “debunk” camp (no exotic injury, no oxidative stress evidence in rigorous testing) holds the high ground in official/government-backed research as of now, while alternative theories linger in investigative journalism and minority expert views. If new 2026 data emerges, it could shift again!

Should I look for any specific 2026 reportsregarding those dissenting voices or the Norwegian self-experiment?

This is all very reassuring, but the Frey effect is real though? And how many economic resources have been invested in researching related topics, such as active denial system, LRAD, non Lethal Weapons, and I reckon, direct energy weapons as well since the Frey effect probably was documented?

Yes, the Frey effect is 100% real. It was first scientifically documented by neuroscientist Allan H. Frey in 1961–1962 (published in the Journal of Applied Physiology), with dozens of subsequent peer-reviewed studies in humans and animals confirming that pulsed microwaves cause thermoelastic expansion in head tissue, producing audible clicks, buzzes, or knocks via bone-conducted pressure waves to the cochlea—no external sound required.

Economic resources invested in related topics (ADS, LRAD, non-lethal weapons, directed-energy weapons/DEW) since the 1960s have been substantial but mostly unclassified figures from the last 20–25 years total several billion USD globally, with the US leading:

• Directed-energy weapons (DEW) overall (lasers, high-power microwaves, including Frey-inspired concepts like MEDUSA): US DoD requested ~$790 million for unclassified DE programs in FY2025 (down from $1.1 billion appropriated in FY2024); one 2025 report cites $2.3 billion US allocation that year. Global DEW market was ~$7–8 billion in 2025 and is projected to reach $20–39 billion by 2030–2035 (CAGR 15–23%). Cumulative US investment since the 2000s (post-Frey military interest) is in the low billions; early 1960s–1990s research (e.g., DARPA Pandora, microwave-hearing patents) was far smaller-scale and often classified.
• Active Denial System (ADS) (millimeter-wave “heat ray,” non-lethal microwave crowd control): Developed 2002–2007 under DoD’s Joint Non-Lethal Weapons Program; single military-grade units cost ~$5 million each, with multi-million-dollar contracts for components and testing.
• LRAD (Long-Range Acoustic Device) (“sound cannon” for non-lethal hailing/escalation-of-force): Recent US military orders alone include $2.5 million (2025) and $9 million (Army CROWS integration); total program investment is in the tens of millions since commercial launch ~2003.
• Joint Non-Lethal Weapons Program (JNLWP) (overarching DoD effort since ~1997, covering ADS, acoustic, and early microwave auditory work): Annual budgets in the tens of millions, supporting transition from research to fielding.

In short: Post-1960s Frey documentation sparked quiet military curiosity (patents, small contracts), but real money flowed from the 1990s onward as non-lethal/DEW programs scaled—hundreds of millions annually now, driven by counter-drone, crowd-control, and area-denial needs. Much more remains classified.

Would you like me to look up more details on the MEDUSA project or other Frey-inspired military patents?

Bring me then the etymology of the Frey name(like begbie in trainspotting might have said it)!

Slektsnavnet Frey (som i Allan H. Frey, fyren som oppdaget mikrobølge-hørselseffekten) er av tysk/sveitsertysk opprinnelse, avledet fra middelhøytysk vrī (eller vri), som betyr “fri” – spesifikt et statusnavn for en fri mann (ikke en trell eller livegen i føydalsystemet), egentlig middelalderens svar på “ingen herre eier meg, skjønner du?”. Det er vanlig i tyskspråklige regioner, med varianter som Frei, Freye eller Fry.

Som fornavn eller mytologisk referanse (som den norrøne guden Frøy/Frey), kommer det fra norrønt Freyr, som betyr “herre” eller “mester” (fra protogermansk frawan, til syvende og sist urindoeuropeisk pro- “fremst/høvding”). Guden Frøy handlet om fruktbarhet, velstand, godt vær og å stå på – ikke akkurat “fri”, men adelig og i ledelsen.

Så, avhengig av konteksten: etternavn = “frifant”, gud/navn = “herskkapelig fruktbarhetskonge”. Uansett har det den gamle germanske tyngden i seg.

Vil du at jeg skal sjekke om det finnes noen koblingermellom navnet Frey og skotske varianter, siden du nevnte Trainspotting?