Will Van Derveer
Will Van Derveer, MD, is a physician working in the field of mental health. His published research includes an investigation into skill retention among Wilderness First Responders, published in the journal Wilderness & Environmental Medicine.
24 claims checked on air: 3 context 3 contradicted 1 overstated 14 supported 3 unverified 4 flagged
What they said on air - contradicted
Quinolinic acid circulating in the gut contributes to increased gut permeability (leaky gut).
"When quinolinate circulates in the gut, it can contribute to leaky gut, right?" (said at 0:37:05)
The speaker claims that circulating quinolinic acid (quinolinate) in the gut contributes to increased gut permeability ("leaky gut"). However, recent preclinical evidence contradicts this claim, showing that quinolinic acid actually helps preserve and reinforce intestinal barrier integrity. In a mouse model of sepsis-induced intestinal injury, quinolinic acid (produced via tryptophan metabolism by gut bacteria) was shown to activate the aryl hydrocarbon receptor (AhR) pathway and downstream Wnt/β-catenin signaling, thereby mitigating intestinal injury and promoting gut barrier integrity rather than compromising it.
Quinolinic acid in systemic circulation causes the activation of macrophages and activation of microglia in the brain.
"And quinolinate can circulate in the in the serum, you know, throughout the body causing activation of macrophages and in the brain microglia as you were talking you've talked about a lot and written about." (said at 0:37:15)
The speaker reverses the primary biological relationship and mischaracterizes the transport dynamics of the kynurenine pathway. Quinolinic acid is primarily an end product synthesized and released by already-activated macrophages and microglia in response to inflammatory stimuli (such as interferon-gamma or lipopolysaccharide), rather than being the systemic agent that initiates macrophage and microglial activation. Furthermore, peripheral quinolinic acid poorly crosses an intact blood-brain barrier; central neuroinflammation and local quinolinic acid production in the brain occur primarily when systemic precursor molecules like kynurenine cross the blood-brain barrier and are locally metabolized by brain-resident microglia and perivascular macrophages.
- context: Kynurenine pathway metabolism in human blood-brain-barrier cells: implications for immune … (Journal of neurochemistry 2008) · cited 109x in the literature
"the basolateral secretion of excess KYN can be further metabolized by perivascular macrophages and microglia with synthesis of quinolinic acid. The results point to a mechanism whereby a systemic inflammatory signal can be transduced across an intact BBB to cause local neurotoxicity." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Beta-trace Protein as a new non-invasive immunological Marker for Quinolinic Acid-induced … (Scientific reports 2017) · cited 22x in the literature
"Quinolinic acid, a macrophage/microglia-derived excitotoxin fulfills a plethora of functions such as neurotoxin, gliotoxin, and proinflammatory mediator, and it alters the integrity and cohesion of the blood-brain barrier in several pathophysiological states." (abstract, introduction, passage verified)
pubmedfull study (doi) - contradicts: Quinolinate as a Marker for Kynurenine Metabolite Formation and the Unresolved Question of… (Frontiers in immunology 2020) · cited 92x in the literature
"Intracellular Quin levels increase dramatically in response to immune stimulation [e.g., lipopolysaccharide (LPS) or pokeweed mitogen (PWM)] in macrophages, microglia, dendritic cells, and other cells of the immune system." (abstract, results, passage verified)
pubmedfull study (doi)
Ketamine acts as a competitive antagonist at the NMDA receptor.
"Ketamine competitively uh blocks the NMDA receptor." (said at 0:37:43)
Ketamine is not a competitive antagonist at the N-methyl-D-aspartate (NMDA) receptor. It acts as a non-competitive (uncompetitive) open-channel blocker, binding to a site inside the ion channel pore rather than competing with glutamate or glycine for their ligand-binding sites on the receptor.
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