Orch OR has been criticized both by physicists and
neuroscientists, He has expressed skepticism that any new physics can resolve the
hard problem of consciousness and argued that quantum theories of consciousness suffer from the same weakness as more conventional theories. Just as he has argued that there is no particular reason why specific macroscopic physical features in the brain should give rise to consciousness, he also holds that there is no particular reason why a specific quantum feature, such as the EM field in the brain, should give rise to consciousness. In 2009, Reimers et al. and McKemmish et al. published critical assessments. Earlier versions of the theory had required tubulin-electrons to form either
Bose–Einsteins or
Frohlich condensates, and the Reimers group noted the lack of empirical evidence that such could occur. Additionally, they calculated that microtubules could only support weak 8 MHz coherence. McKemmish et al. argued that
aromatic molecules cannot switch states, because they are delocalized, and that changes in tubulin protein-conformation driven by
GTP conversion would result in a prohibitive energy requirement.
Endogenous ferritin quenches microtubule radiance, which may prevent generation of ultraviolet biophotons While some of the studies mentioned above purport to show superradiance and an influence of anesthetics on decreasing excitation diffusion through microtubules, those studies were performed under artificial conditions that failed to include proteins associated with microtubules like
ferritin, which quenches microtubule superradiance. Evidence published prior to those studies establishes that ferritin interacts with microtubules in vivo and is essential for microtubule stability and function. For instance, those studies overlooked that: • Studies of biophotons in the human body fail to find any evidence of
ultraviolet (UV)
biophotons. In contrast, at least one of the studies cited above that is relied on as evidence of microtubule superradiance in support of Orch-OR relies on earlier studies of UV biophotons measured in single-celled organisms like
E. coli and respiratory deficient yeast as the basis for its contention that such biophotons are present in cells. That study also used
UV-vis equipment with a light source that can generate 1020 photons per second, which is not representative of neurons' environment. • Ferritin in the human body absorbs UV from external sources at least in the skin and in the cornea, where the levels of UV photons are much higher than measured biophoton levels of UV even in
E. coli and yeast. Endogenous ferritin in neurons would absorb UV biophotons that might be emitted from chemical processes (at levels that are too low to measure), and those UV biophotons would not even reach microtubules to cause superradiance or energy transport. • Ferritin contains tryptophan residues, the same material in microtubules that is supposed to cause microtubule superradiance. According to one of the studies cited above, microtubule superradiance is based on special configurations of tryptophan residues. The failure of that study to consider additional ferritin tryptophan residues in the vicinity of microtubule tryptophan residues means that the study is not relevant to cellular environments that include ferritin (which is basically every cell). As noted above, ferritin perturbs tubulin in the vicinity of tryptophan residues, which invalidates an
a priori assumption of that study. • Ferritin has stronger ionic interaction with microtubules than the anesthetics that were used in one of the studies cited above and has electrical and magnetic properties that those anesthetics lack. Even if anesthetics interact with microtubules, ferritin has stronger interactions with microtubules, which may explain why ferritin is able to quench microtubule fluorescence. In summary, experiments trying to demonstrate microtubule superradiance involved unrealistic levels of UV light and artificial environments, and excluded cellular substances that would prevent microtubule superradiance and energy transport.
Neuroscience Biology-based criticisms have been offered, including a lack of explanation for the probabilistic release of
neurotransmitters from presynaptic
axon terminals and an error in the calculated number of the tubulin dimers per cortical neuron. In 2014, Penrose and Hameroff published responses to some criticisms and revisions to many of the theory's peripheral assumptions, while retaining the core hypothesis. ==See also==