I am retired Emeritus Professor at The University of Arizona, Tucson, Arizona and Senior Scientist, Quantum Life Technologies, San Francisco, California
Greenbrae, California
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Stuart Hameroff retweeted
Orch OR and Penrose Biosi and microtubule resonance could they be linked? Wont it be a dream project? Thanks @JosephJacks_ and @StuartHameroff for kwnsfk27.r.eu-west-1.awstrac… our new paper just out
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Stuart Hameroff retweeted
What a panel! @M31Capital hosted the kind of afternoon that put microtubules, psi data, uap and near death testimony on the same stage without collapsing into lab coat dismissiveness or woo. Elucidating. @StuartHameroff @Jason_Jorjani @MaxDerakhshani
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There’s another way to look at it. Consciousness came first, and life (aromatic hydrocarbons) accessed pleasure and developed/evolved to optimize feelings. How could consciousness exist in the universe without life or brains? (Penrose OR). How can it exist now WITH life and brains? (Orch OR).
sciencedirect.com/science/ch…
I’m not sure why anyone would think consciousness has no effect on the brain, but it’s good to see evidence that it does. Consciousness evolved to serve a function. It isn’t here for our entertainment.
dailyneuron.com/consciousnes…
#neuroscience
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Everything overlaps anatomically and must be ‘disentangled’? Sounds like a hologram where the raw information is distributed as interference patterns until reilluminated by a coherent laser-like source. Microtubules could be the laser-like source of coherent brain waves not just in EEG range but faster, quantum oscillations in megahertz and gigahertz.
I’d bet a 2-d cut or surface of a 3-d dynamical (4-d) hologram would probably look like an EEG.
Earl, could the MIT hotshots put an optical EEG cap on the Princess Leah hologram from Star Wars?
Averaging brain activity can hide important details. Here, they separated overlapping processes in real time. Signals of attention and preparation appeared across multiple brain regions and predicted participants’ accuracy and confidence.
biorxiv.org/content/10.64898…
#neuroscience
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Very pleased to speak at The Physics of Consciousness Friday at DeepTech week in Austin, especially alongside the great Hal Puthoff.
A bonus surprise speaker has joined the lineup, none other than Hal Puthoff
Hal joins @Jason_Jorjani , @StuartHameroff , Thomas Brophy, James Tagg and @MaxDerakhshani
I think this is shaping up to be one of the most interesting and frontier events @deeptechweek has ever hosted
thanks again to @M31Capital for making it possible
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Much irony here. Biology desperately needs unitary oneness, and consciousness needs unitary self and spatiotemporal binding, both provided by quantum coherence and entanglement. But decoherence is too fast in ‘warm, wet and noisy biology’ everyone says. How fast is too fast?
The article briefly mentions Nobel laureate Sir Roger Penrose ‘s OR
(objective reduction) idea that microtubules inside neurons have sequences of quantum collapses which resulted in consciousness. The article also says few neuroscientists take it seriously. Thats true but few neuroscientists have a clue about consciousness, following cartoon ‘neurocomputation’ at one slow frequency range.
Actually I told Roger about microtubules in the early 90s and we developed the Orch OR theory of consciousness mid 90s which now has by far more explanatory power, biological specificity and experimental validation than all other theories of consciousness combined. That’s mostly because anesthesia acts by quantum interactions with microtubules academic.oup.com/nc/article/… and because none of the cartoon neuron theories have any real evidence whatsoever.
Greg Scholes and I were co-authors on a paper showing warm temperature quantum states in microtubules lasted 10^-8 secs and were dampened by two different anesthetics pubmed.ncbi.nlm.nih.gov/3696…
A warm temperature organic polymer gel ‘(brain jelly) sustained a quantum soliton-polariton condensate for 5 milliseconds. pubmed.ncbi.nlm.nih.gov/4170…
That’s 10^-3 to 10^-2 secs
But how brief is too brief?
Lets assume 10^-8 secs coherence/decoherence time as in our paper. In Orch PR conscious moments occur time t=h/E where h is Planck-Dirac constant and E the gravitational self energy. At time t = 10^-8 secs, E is 10^16 tubulins (10^20 in the brain). But cognitive processes, EEG etc are much slower. Roger and I proposed megahertz waves interfered in negative resonance to create slower EEG waves pubmed.ncbi.nlm.nih.gov/2407… after all these years we don’t understand EEG. Maybe it’s part of a microtubule collective oscillators as proposed in honeybees pubmed.ncbi.nlm.nih.gov/3465…
The article mentioned the vast scales in living systems and this may be solved by microtubules acting as time crystals
ingentaconnect.com/content/i…
Finally, Greg Scholes conjectures 3 1/2 billion years of evolution allowed us to get smart enough to use quantum math to explain classical brain activities. It’s more likely that Penrose OR in polyaromatic hydrocarbons produced by stars and carried to earth by meteorites generated pleasure and the aromatics arranged to optimize good feelings sciencedirect.com/science/ch…
Such early systems could have been helical aromatic time crystals.
It’s sad to see Greg Scholes surrender.
Scientists have a history of trying — and failing — to link biology and quantum mechanics. The real connection between them may be in the math. quantamagazine.org/biology-m…
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Nice! Pretty much everything in this approach is based on nested hierarchy, scale and phase/interference with persistence of patterns. Every neuron and glial cell in this approach is filled with microtubules acting as polyatomic time crystals which can entangle and form nested hierarchies, transcend scale and encode patterns.
This is a job for polyatomic microtubule time crystals ingentaconnect.com/content/i…
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I really don’t know what your theory is but it seems based on cartoon neurons and neuro anatomy . What evidence do you have? What explanatory power? And I think dividing consciousness into various components is post modern deconstruction of a grand unified concept in an attempt to get rid of it. Just explain awareness and I’ll be impressed.
A scoping point that might actually help the conversation: my framework separates three things that usually get run together.
Awareness — why there is phenomenal experience at all — I bracket explicitly, much as you set aside the hard problem when discussing the Oxford result.
Address — that there is a located point of view
Occurrence — that this point of view is actively maintained rather than simply given — are where the anesthesia evidence actually lives.
Both of our theories, I'd argue, are ultimately claims about Occurrence: what maintains the state, and what happens pharmacologically when the maintaining stops.
Framed that way, the disagreement between us becomes a tractable question — what kind of evidence decides between two accounts of the maintaining, rather than two accounts of the mystery.
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We’re way outnumbered and considered a threat to cartoon neuron theories so there’s a lot of phoney criticism which has been refuted. So please be specific. Theres way more evidence supporting Orch OR than all other theories of consciousness combined.
For one example see academic.oup.com/nc/article/…
Is there any experimental proof for orch or cuz everything I see about it says it’s been heavily discredited
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Anesthesia was originally defined as loss of 1) consciousness, 2) memory formation and 3) movement. In the 80s/90s Dennett, Churchland and eliminative materialists started questioning whether consciousness existed or was an illusion (to whom I’m not sure). Authorities in anesthesiology including Ted Eger at UCSF and Keith Miller at Harvard wanted to be ‘scientific’ and said, essentially, since we can’t measure consciousness and philosophers say it doesn’t exist let’s define anesthesia on what we can measure which is movement (as MAC was defined in animals and neither memory nor consciousness could be assessed). They started calling it ‘immobility’. I thought that was chickenshit and have yet to see an illusionist philosopher volunteer to have surgery without anesthesia.
It is true that a guy at UC Davis showed in animals that if you sever the brain stem or high spinal cord the animals didn’t move when stimulated below the lesion. Big surprise. I anesthetized many quadriplegics and they definitely required anesthesia (mass autonomic reflexes for one reason). If what you’re suggesting were true they’d already be unconscious. The chickenshit renaming led to assertions that anesthesia just caused immobility and amnesia and patients were awake and suffering but didn’t remember. That’s bullshit too because ‘light anesthesia’ is marked by autonomic warning signals.
As far as weak binding to a humongous number of receptors, tubulin is NOT
‘Off Target’ for consciousness, But that’s only because consciousness is a quantum mechanism and weak quantum binding to any part of a unified quantum state is sufficient to disrupt it.
I’d say GABA_A receptors are off target sites despite MAC being affected by
mutations because not all anesthetics bind to it. Before propofol, drug companies tried pure GABA_A receptor agonists like midazolam for induction of anesthesia and it didn’t work. Some patients didn’t go to sleep despite huge doses, and when they did they responded to stimuli.
Anirban’s work hasn’t been replicated because he’s ten years ahead of everybody, However megahertz and gigahertz triplets can be detected from scalp in humans and correlates with mental states. We have a poster presentation at Society for Neuroscience in Washington DC on November 17. It’s
called ‘Introducing the DDG (dodeconogram)’ and reports on megahertz and gigahertz changes with mental states. Come on by.
Eger 2008 is about immobility — response to noxious stimulus, substantially a spinal cord phenomenon — not the neural correlates of unconsciousness. Different endpoint, different circuit. It doesn't carry the weight you're putting on it.
The occupancy math doesn't get you causation. A weak, promiscuous ligand binding a million abundant off-targets more often than a rare high-affinity one isn't evidence the low-affinity binding does anything — that's true of nearly every drug in pharmacology. GABA_A still has the clean causal lever: one point mutation, behavioral resistance. Nothing on the tubulin side clears that bar.
And on Anirban — has anyone outside his own lab replicated it? First report from an invested lab isn't proof, it's a claim waiting on the step everything else here has skipped too.
This is the actual asymmetry: PVC doesn't need any of these unreplicated results to hold. GABA_A/NMDA gating the thalamocortical loop off from live proprioceptive-vestibular return is already-established pharmacology — Occurrence just tracks what happens to ρ and α/θ when that loop is cut. Falsifiable with data that already exists, no new physics required. Orch-OR needs Anirban's coherence times to replicate, needs a causal tubulin study that doesn't exist yet, and needs an Oxford result that hasn't tested OR at all. That's three unclosed loops propping up one conclusion. I only need one, and it's closed.
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All anesthetics acting on one target was the conclusion of Meyer and Overton who also correlated anesthetic potency with solubility in olive oil. This implicated lipid membranes but later settled on oil-like regions near aromatic rings of amino acids tryptophan, phenylalanine and tyrosine. inside proteins. Which protein? Decades of searching membrane receptor and ion channel proteins came up empty and the leading researchers Ted Eger et al (2008) concluded no single membrane protein or group of membrane proteins sufficed pubmed.ncbi.nlm.nih.gov/1871…
But rather than consider microtubules they got rid of Meyer and Overton and resorted to handwaving emergence arguments. All anesthetics. one target only works for tubulin.
Binding: Nick Franks told me anesthetics bind GABA_A receptors a thousand times stronger than tubulin. But there were a million times more tubulins per neuron than GABA_A receptors so a thousand times more anesthetic bound to tubulin than to GABA_A receptors. And besides we’ve shown experimentally anesthetics block warm temperature quantum effects in microtubules pubmed.ncbi.nlm.nih.gov/3696…
GABA_A receptor mutations do increase sensitivity to anesthesia but so do a lot of things. Microtubule stabilizing drugs make humans and animals resistant to anesthesia.
As far as a biological quantum condensate Anirban just proved it !
And if you’re saying thalamus isn’t always necessary then you have several varieties of Consciousbess to explain when you can’t explain any of them. It’s better to just say Orch OR is happening inside brain neurons and glia
Meyer-Overton tracks shared physicochemistry (hydrophobic pocket + lipid-solubility scaling), not a shared literal target — ketamine/xenon/N2O barely touch GABA_A and work through NMDA instead. So "all anesthetics, one target" was never quite true on either reading. Doesn't help tubulin, doesn't hurt the protein account.
A million low-affinity tubulins binding anesthetics weakly is occupancy, not causation. GABA_A has the actual causal test already run: anesthetic-insensitive knock-in mice become behaviorally resistant. No tubulin mutation clears that bar. And "decoherence disrupts the whole condensate" assumes the condensate to explain why the binding matters — that's circular, not corroborating.
Smell's a real point, just not against this. PVC doesn't claim thalamic gating of all conscious content — it's scoped to the P-V-C loop specifically, and proprioceptive/vestibular afference is thalamically relayed regardless of what olfaction does. Awareness in general is explicitly bracketed here, not claimed solved.
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Good question but not really. You’re quite right that anesthetic solubility correlates with both lipid membranes and hydrophobic aromatic ring regions inside proteins. Lipid membranes are fluid and uncinstrsuned-a bulk solvent as you suggest. Proteins have smaller cavities with fewer degrees of freedom. See Figure 6 middle in this paper
frontiersin.org/journals/mol…
You’ll see 6 anesthetic molecules among 86 quantum-friendly aromatic rings. Adjacent rings can only be in two arrangements with each other so it’s not fluid, more geometric
The split between a broad solubility correlation and a specific binding-site mechanism is the key here. Stereoselectivity and cutoff effects are hard constraints; any microtubule account has to explain them quantitatively, not just remain compatible with partitioning.
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Meyer-Overton tells us that all anesthetics act on the same target (a protein). Many but not all anesthetics bind GABA_A inhibitory receptors, but some open them and some close them.
Same with other membrane receptors and channels. Microtubule tubulin proteins appear to bind all anesthetics though low affinity compared to GABA_A receptor binding. But there are about a million more tubulins per neuron than GABA_A receptors. And they’re in a quantum condensate so decohering any part would disrupt the whole.
Ignoring Meyer -Overton is like ignoring the Rosetta Stone if you’re trying to understand ancient Sumerian.
And thalamus can’t be necessary for consciousness because conscious smell doesnt go through thalamus.
Anesthetics hit GABA_A/glycine/NMDA channels at the synapse — that part's settled pharmacology, not in dispute. What that does functionally is decouple the thalamocortical loop from proprioceptive-vestibular afference: cortex stops integrating the ongoing P-V return signal even though the signal itself (muscle spindle, GTO, otolithic, canal input) is still arriving. Occurrence, on this account, isn't a property generated inside tubulin — it's what happens when a return operator ℛ keeps regulating the α/θ ratio ρ against a live proprioceptive-vestibular reference. Cut the cortical side out of that loop and ρ has nothing left to regulate. α/θ collapses or flattens not because a quantum process in the cytoskeleton switched off, but because the regulatory loop generating that spectral signature no longer has an input to close around.
That's why anesthesia, sleep, and Ian Waterman’s kind of deafferentation all show family-resemblant EEG signatures without needing a shared molecular substrate — they're different ways of breaking the same loop (cortical gating vs. loss of the input itself), not different doses of the same microtubule effect.
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Anesthetics don’t do biochemistry, they are chemically inert, e.g. xenon. They bind and act by quantum van der Waals dipole couplings with aromatic rings inside tubulin to dampen their quantum oscillations and disrupt superposition.
Thats biophysics.
I’m well award of the water ordered on microtubule surfaces, inside the cylindrical core and on the exterior.
In 1994 I coauthored this paper predicting superradiance in microtubules due to quantum oscillations of water in the hollow core
pubmed.ncbi.nlm.nih.gov/7919…
No doubt ordered water is important but I’m pretty sure the quantum optics in the aromatics regulate the oscillations of C termini and other charge carriers on tubulin surface which interacts with water. The dog wags the tails.
Do you know microtubules assemble from individual tubulins by entropy into awesome quasi crystal structure? In solution each tubulin binds and orders 20 water molecules. Assembled tubulins can bind only 8 tubulins so there’s a net disordering despite the crystallization.
Of course I disagree. You offered a biochemical answer and missed the biophysics reality.
When you dismiss the water dielectric constant based purely on the poor water-solubility of anesthetics is a fundamental biophysical mistake that treats protein structures as if they exist in a vacuum. While anesthetics preferentially partition into the non-polar, hydrophobic pockets of tubulin, their very entry into these pockets is thermodynamically driven by their exclusion from the highly polar aqueous phase surrounding the microtubule.
Microtubules are not dry structures, yet your reply acts like they are; they are highly charged polyelectrolytes completely encased in an asymmetric, ultra-ordered, and highly polarized layer of interfacial water molecules. This constrained water layer collapses the local relative dielectric constant from its bulk value of 80 down to approximately 9 right at the protein interface, establishing the precise electromagnetic boundaries required for microtubules to function as transmission lines for electrical and acoustic oscillations. On these grounds alone your theory collapses. And the data on this is overwhelming.
By inserting themselves into the protein-water boundary, anesthetics directly disrupt the collective organization and phase transitions of this interfacial water. To argue that water's dielectric properties have nothing to do with anesthesia ignores the fact that shifting the local dielectric constant fundamentally alters the electromagnetic shielding, the capacitance, and the localized electric fields that govern the entire structural and vibrational state of the microtubule itself. Stu you have to be better than this.
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Meyer-Overton tells us the solubility compartment in which anesthetics bind by quantum dipole couplings to selectively block consciousness. That turns out to be oil-like or fat-like regions in membranes, nucleic acids and proteins. The answer ( where anesthetics act) is proteins.
I totally agree lipid theories of anesthetics fail because of cutoff and stereo selectivity but that doesn’t rule out tubulin proteins which each have about 6 anesthetic binding sites per tubulin among its 86 aromatic rings. pubmed.ncbi.nlm.nih.gov/3578…
nature.com/articles/s41598-0…
Yes anesthetics bind to GABA receptors and others also. But they ACT on tubulin according to genomics, proteomics, optogenetics and pharmacodynamics.
Decoherence times-Yes we’ve shown fairly lengthy microtubule quantum coherence times with longer results in the pipeline. Anirban’s ’brain jelly’ has room temperature phonon-polariton quantum condensates lasting 5 milliseconds. iopscience.iop.org/article/1… That’s 200 hertz, almost EEG range. But Orch OR only needs, say microsecond Orch OR coherence times, in megahertz. We claim those waves interfere in negative resonance to give slower and slower frequencies. That’s how microtubules generate the EEG. You’re welcome.
pubmed.ncbi.nlm.nih.gov/2407…
True Roger’s OR collapse hasn’t been proven but the recent experiment connecting quantum physics and Einstein’s general relativity/quantum gravity confirmed Roger’s prediction 35 years ago. And sets the stage to test OR collapse soon. ox.ac.uk/news/2026-08-28-sci…
We HAVE proven Orch, the quantum biological conditions for Orch OR
Yes IIT and GNW have predictions about where in the brain activity will occur for various conditions which sometimes come true. But:
1) we don’t know what fMRI is telling us
2) EEG probably comes from microtubules, and there are megahertz and gigahertz microtubule oscillations there anyway
3) identifying gross anatomical areas without an account of what physiology is causing it nor why or how that relates to consciousness is ok, kinda like
‘pin the tail on the brainmap’.
Meyer-Overton is a historical correlation, not a mechanism — Franks & Lieb (1984) showed anesthetics inhibit a lipid-free enzyme at clinical concentrations, and stereoselectivity + the cutoff effect rule out a bulk lipid/tubulin target outright. Anesthetics act at specific hydrophobic pockets on GABA_A/glycine/NMDA channels. That's not a competing interpretation, it's the reason the field left the lipid theory 40 years ago.
And "more explanatory power than every other theory of consciousness combined" fails your own field's basic test. Your best-case recalculated decoherence time (~10⁻⁴–10⁻³s) is still short of the ~25ms Orch-OR needs, resting on a collapse mechanism with zero independent confirmation. GWT and IIT, whatever their flaws, are at least tied to decades of lesion and neuroimaging data. Confidence isn't evidence.
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Anesthetics are poorly soluble in water, highly soluble in nonpolar regions and act near aromatic rings in microtubules. Most water in cells is ordered by charged surface dynamics of microtubules and other cytoskeletal structures. There are some ‘clathrate’ effects of anesthetics on water-protein interfaces but they aren’t relevant to anesthetic action. Orch OR has more explanatory power, biological specificity and experimental support than all other theories of consciousness combined. Do you disagree?
Anesthesia all operates ona changing dielectric constant of water. MT can do nothing without water. The physics is clear. ORCH-OR is folly. This is why one side of the MT has a different size then the other. See Me Wan Ho work why.
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Yes anesthesia blocks long range and cross-scale couplings most likely due to microtubule quantum entanglement and time crystal behavior.
Meyer (1897) and Overton (1903) showed all anesthetics act on one target and Eger et al (2008) ruled out all membrane proteins pubmed.ncbi.nlm.nih.gov/1871…
Meanwhile evidence points to microtubule quantum effects mediating selective anesthetic-induced loss of consciousness and purposeful behavior
academic.oup.com/nc/article/…
Nonetheless the anesthesia mafia continues to bark up all the wrong trees while beating dead horses of membrane protein-mediated anesthesia.
Anaesthesia fragments the emergent multiscale organization of neural dynamics, demonstrating that consciousness relies on how activity is structured rather than just its magnitude. By using dynamical independence to quantify these multi-scale relationships, the work shifts the focus from simple brain activation levels to the specific information-theoretic dimensionality of coordinated processes.
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So not only memory and categorization are distributed in the brain, so is navigation! Is there holography going on in the brain, possible through interference of coherent waves? But slow EEG waves unlikely to have the resolution so it’s likely from faster coherent waves (megahertz, gigahertz…) from microtubules, particularly mixed polarity dendritic-somatic microtubules ideal for interference. These mixed polarity microtubules are found only in neuronal dendrites and soma pubmed.ncbi.nlm.nih.gov/3578…
Navigation isn't just in the hippocampus. It's encoded across the whole brain, suggesting navigation-related signals are broadly distributed rather than localized.
Brainwide representation of navigation
doi.org/10.64898/2026.08.29.…
#neuroscience
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Yes tsc2026.org
offers online streaming of Plenary talks and featured workshops
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The Science of Consciousness 2026 is 3 weeks away, October 11-16. We have 700 registrants, and group rooms and bungalows at Paradise Point Resort in Mission Bay, San Diego are almost filled and close in one week. Program and other info at tsc2026.org
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