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moderate preclinical evidence ALC plays a fundamental role in mitochondrial function by facilitating the transport of long-chain fatty acids across the inner mitochondrial membrane for -oxidation and ATP production.[7] Dietary supplementation with ALC counteracts age-related alterations of mitochondrial biogenesis, dynamics, and antioxidant defenses in the brain, increasing levels of PGC-1, PGC-1, NRF-1, and TFAMkey regulators of mitochondrial biogenesis.[8] ALC also counteracts the age-related increase of deleted mitochondrial DNA and restores mitochondrial content and function.[8][9] In hypoxic conditions, ALC-mediated neuroprotection is attributed to ERK1/2-Nrf2-regulated mitochondrial biosynthesis, effectively protecting hippocampal neurons from mitochondrial dysfunction, excitotoxicity, and neurodegeneration.[10] Combination Strategies for Mitochondrial Dysfunction: ALC 1,500-3,000 mg/day + CoQ10 100-300 mg/day (complementary electron transport chain support) + Alpha-lipoic acid 600 mg/day (complementary metabolic support) + B vitamins (cofactors for mitochondrial enzymes) 3

It prevents the formation of advanced glycation end products (AGEs), which contribute to age-related diseases, such as diabetes, cardiovascular disease, and neurodegenerative disorders (Nagai et al., 2012)

Eggs can help to maintain the required concentration of antioxidants in the body

Recent data reported by the International Diabetes Federation (IDF) in 2021 have demonstrated that the global prevalence of diabetes was estimated at 10.5% (approximately 537 million people) ( Glucagon-like peptide-1 (GLP-1) is an insulin-promoting hormone and can enhance glucose-dependent insulin secretion, inhibit glucagon secretion and delay gastric emptying

Rafael de Cabo (via National Institutes of Health)