Start ASAP (ideally within 24 hours). Tier 1 compounds deliver maximum impact during this critical window. Adjust based on symptom response and medical clearance.
Tier 1 compounds have been tested directly in concussed athletes or military personnel with quantified recovery outcomes. Tier 2 compounds have good mechanistic support and RCT evidence in TBI or athletes. Tier 3 compounds are promising but lack human concussion RCTs—use only if Tier 1/2 inadequate.
• In a quasi-randomized study of adults with mild TBI, oral NAC (4 g load then 2 g twice daily for 4 days and 1.5 g twice daily for 3 days) added to standard care was associated with significantly lower Rivermead Postconcussion Questionnaire scores at 7 and 30 days versus standard care alone, supporting NAC as an early neuroprotective adjunct in mild TBI.
• Preclinical and battlefield data (including a PLOS One trial in blast-exposed soldiers) suggest that early NAC use can reverse cognitive and vestibular deficits and reduce oxidative injury after blast and blunt mTBI, providing mechanistic plausibility for its use in sports concussion.
• A double-blind randomized controlled trial in collegiate athletes with sport-related concussion found that riboflavin 400 mg daily for 14 days shortened mean time to clinical recovery from 22.2 days with placebo to 9.9 days with riboflavin, without major safety signals.
• Clinical trial registrations and follow-up analyses in concussion and post-traumatic headache further support riboflavin's role in mitochondrial support and headache reduction in this population.
• A multi-year pilot study in adolescents and young adults (ages 11–34) with concussion reported a dose–response relationship between BCAA intake and symptom improvement, with higher doses linked to greater reductions in symptom scores and improvements in physical activity and sleep measures.
• The Minds Matter program at CHOP describes BCAAs as a targeted pharmacologic tool in concussion care, not just a sports supplement, emphasizing their role in neurotransmitter balance and recovery of function after concussion.
• A randomized study of adolescents with acute concussion found that oral magnesium supplementation, when added to standard care, improved post-concussion symptom severity over a 5‑day period compared to standard care alone, suggesting benefit in the early symptomatic phase.
• Reviews and NIH monographs on nutrition and TBI highlight that serum and brain magnesium decline rapidly after injury and that replacement may attenuate excitotoxic damage and migraine-like headache after TBI.
• Preclinical TBI models show that DHA-rich omega‑3 supplementation preserves axonal structure, reduces β-APP–positive injured axons, and improves cognitive outcomes after experimental brain injury.
• Emerging human work in contact sports (e.g., American football) suggests that omega‑3 supplementation over a season may blunt increases in serum neurofilament light chain and other neurotrauma biomarkers associated with repetitive head impacts.
• Multi-center observational data indicate that vitamin D deficiency at the time of TBI is associated with worse functional recovery and higher mortality, suggesting that adequate vitamin D status may influence resilience and outcome after brain injury.
• Preclinical studies and small clinical trials suggest that vitamin D can attenuate post-TBI neuroinflammation and neuronal loss, and supplementation has been associated with improvements in inflammatory markers and early neurological scores in some brain injury cohorts.
• Animal models of TBI demonstrate that chronic creatine supplementation reduces cortical damage by roughly 36–50%, preserves ATP, and stabilizes mitochondrial function, indicating a strong neuroprotective effect at the tissue level.
• A 2025 scoping review of creatine in TBI and collision-sport athletes concluded that creatine appears to reduce tissue damage and support energy metabolism after brain injury, with early human data in moderate–severe TBI and athletes supporting further trials.
• A clinical trial in patients with moderate–severe TBI showed that zinc supplementation (initial parenteral then enteral) improved Glasgow Coma Scale scores, visceral protein markers, and 1‑month survival compared with patients receiving only adequate zinc, suggesting zinc as a therapeutic adjunct.
• Preclinical and translational work indicates that zinc deficiency worsens neuronal death and behavioral deficits after TBI, whereas appropriate supplementation improves resilience and may protect against subsequent brain insults.
• Experimental models of TBI and ischemic brain injury show that taurine supplementation improves neurological scores, reduces brain edema, and attenuates microglia-driven neuroinflammation, consistent with a broad neuroprotective role.
• Mechanistic studies demonstrate that taurine reduces oxidative stress in neurons in part by inhibiting NADPH oxidase–mediated reactive oxygen species production, supporting its use as an adjunct antioxidant.
• Multiple animal TBI models show that curcumin reduces oxidative stress, edema, and neuronal apoptosis and improves histologic and behavioral outcomes, acting through NF‑κB, Nrf2, and other inflammatory pathways.
• A systematic review of curcumin-based delivery systems for TBI-related conditions concludes that curcumin is mechanistically promising but human concussion trials are still lacking; recent murine models of repetitive TBI with turmeric/curcumin pretreatment further support this biologic plausibility.
Search your current medications to identify potential interactions with Impact Shield protocol compounds. Always consult your physician before starting supplements.