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5 Antioxidants targeting oxidative stress and neuroinflammation in ASD Besides excessive levels of oxidative stress and pro-inflammatory molecules, ASD patients are also distinguished for their nutritional deficits

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Key mechanisms: Activates AMPK (the body's master metabolic switch) Restores mitochondrial efficiency more ATP produced per unit of substrate Improves fat oxidation at aerobic paces (better fuel usage during training) Enhances insulin sensitivity Upregulates stress response pathways More cellular energy available during training Better endurance and output across a 5-day training week Improved fat-to-muscle composition (body recomp effect) Supports lean mass preservation during caloric restriction Stimulates collagen and elastin synthesis Activates anti-inflammatory signaling pathways Promotes tissue repair and wound healing Upregulates genes associated with cellular protection Supports extracellular matrix repair Faster recovery from training-induced tissue stress Stronger tendons and ligaments over time Reduced joint inflammation Improved skin quality (significant cosmetic effect) Better soft tissue repair around muscle insertions Mitochondrial decline limiting energy and output MOTS-C addresses this Higher connective tissue stress from heavy volume GHK-Cu addresses this MOTS-C: 500mcg daily, morning (subQ) GHK-Cu: 12mg daily, any time (subQ) Optional add: Tesamorelin 1mg daily for GH axis support and visceral fat reduction NMN/NAD+ provides the raw substrate for mitochondrial reactions MOTS-C improves the efficiency of how mitochondria use that substrate Together they're more effective than either alone for the mitochondrial decline that accelerates muscle loss after 50

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10.1523/JNEUROSCI.18-23-09620.1998 112 LewerenzJ.MaherP.MethnerA