Two predominant theories developed mainly from the competing neuroimmaging data from Franz Vollenweider and Robin Carhart-Harris bring up an important discussion about research methodology.

CH et al.'s research has led to a great deal of discussion but very little of it directly addresses this discrepancy. Most of what the recent media has covered has exclusively focused on Carhart-Harris' findings while ignoring the results Vollenweider et al. have found consistently for decades. This demonstrates that the vast majority of articles on psychedelics are incomplete, inaccurate, or misleading. Psychedelic science should resolve V's hyper-frontality and CH's hypo-frontality before presenting and offering interpretations of psychedelic neuroscience to the public. Any article that presents CH's results without mentioning this issue should be discarded as lacking integrity.

This is the hyper-/hypo- front.

Vollenweider observes mainly increases in frontal brain activity, while Carhart-Harris observes mainly decreases in frontal brain activity.

V uses oral doses with long onset; CH uses intravenous with rapid onset

V uses mostly PET; CH uses mainly fMRI

This paper offers an explanation based on neurovascular effects of psilocybin.

Some notable excerpts:

Evidence suggests negative BOLD signals can have separable haemodynamic and neuronal sources and may occur in the presence of increased neuronal signalling

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5-HT2A receptors are also expressed on both pyramidal cells and inhibitory interneurons, suggesting that agonism of this receptor can have both excitatory and inhibitory effects on downstream neuronal signalling. Cortical inhibitory interneurons are capable of producing both vasodilation and vasoconstriction, providing a mechanism by which reduced synaptic activity may actually be associated with increased CBF.

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The findings presented here are particularly relevant to situations where alterations in brain responses to sensory (e.g. visual, auditory) stimulation are being investigated using neuroimaging, as they demonstrate that serotonergic manipulations may alter the relationship of BOLD signal changes to neuronal activity. To exemplify, in isolation, our haemodynamic (i.e. neuroimaging) data suggests that psilocin increases the magnitude of cortical responses to sensory stimulation. In fact, our concurrent measurement of neuronal response magnitudes suggests that if anything, the opposite is true.

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many interpretations of BOLD-fMRI signal changes assume a monotonic relationship between evoked neuronal and haemodynamic response magnitudes, something we have here demonstrated to be altered by psilocin administration. Furthermore, the alteration in neurovascular coupling we report here might explain, in part, the apparent discrepancy between fMRI and PET findings of decreased CBF and increased glucose metabolism in human studies with psilocybin and related drugs.

Thoughts? What does this mean in terms of interpreting the whole?