Black Seed OilvsShilajit

Thymoquinone is the primary bioactive, providing neuroprotection through multiple mechanisms: it scavenges reactive oxygen species (superoxide, hydroxyl radical, peroxynitrite) and upregulates Nrf2/ARE pathway, increasing glutathione (via GCLC, GSS), superoxide dismutase (SOD1/SOD2), and catalase. It inhibits NF-kB by preventing IkB-alpha degradation and blocking p65 nuclear translocation, reducing neuroinflammation and pro-inflammatory cytokine release. Thymoquinone inhibits acetylcholinesterase (AChE) at the peripheral anionic site, increasing synaptic acetylcholine. It modulates GABA-A receptors (positive allosteric modulation at benzodiazepine site), providing anxiolytic effects. Thymoquinone protects neurons from amyloid-beta toxicity by reducing oxidative stress and inhibiting beta-secretase (BACE1). It reduces tau hyperphosphorylation by inhibiting GSK-3beta and CDK5.

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.