ALCARvsShilajit

ALCAR crosses the blood-brain barrier via the organic cation transporter (OCTN2) more effectively than L-carnitine. In neurons, it is hydrolyzed by carnitine acetyltransferase to donate its acetyl group to coenzyme A, forming acetyl-CoA—which can then be used for acetylcholine synthesis via choline acetyltransferase, effectively providing raw material for the memory neurotransmitter. ALCAR also transports long-chain fatty acids across the inner mitochondrial membrane via the carnitine palmitoyltransferase system for beta-oxidation and ATP production. ALCAR activates nerve growth factor (NGF) signaling, possibly through modulation of NGF receptor (TrkA) expression or downstream MAPK/ERK pathways. It has antioxidant properties, reducing lipid peroxidation in mitochondrial membranes and scavenging free radicals. These mechanisms support cognitive function and neuroprotection.

Fulvic acid is the primary bioactive, acting as an electron shuttle that donates and accepts electrons — enhancing mitochondrial electron transport chain efficiency by facilitating electron transfer at Complex I and II, similar to CoQ10 but through a different (non-enzymatic) mechanism. DBPs (dibenzo-alpha-pyrones) protect CoQ10 from oxidation by scavenging radicals, extending its functional life in the reduced ubiquinol form. The combination increases ATP production in mitochondria. Fulvic acid also chelates minerals (iron, zinc, magnesium) via carboxyl and phenolic groups, forming soluble complexes that transport across cell membranes via divalent metal transporter 1 (DMT1) and other channels, improving bioavailability. It has direct antioxidant effects (scavenging ROS) and anti-inflammatory effects through inhibition of complement C3 activation and NF-kB.