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Given the ancient origin of the Ca 2+ -based signaling, which evolutionary developed earlier than the mitochondrial apoptotic toolkit whose emergence cannot be dated back to the times earlier than eukaryogenesis and acquisition of an endosymbiotic mitochondrion, it can be assumed that the Ca 2+ toolkit takes over a key role in cell death signaling in terminally differentiated mitochondria-free erythrocytes
Third, potency assays should be standardized and linked to the stated mechanism
A study where healthy individuals received a -HB infusion to achieve a concentration of approximately 5.5 mmol/L demonstrated a 14% reduction in brain glucose utilization and a significant 30% increase in cerebral blood flow, with unchanged oxygen consumption [77]
This alone obfuscates anything you can hope to gleam from the study
Studies suggest ascorbic acid derivatives may suppress inflammatory cytokine pathways including interleukin-33, potentially benefiting barrier-compromised skin states
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