Creatine Monohydrate for ALS
Also known as: Creatine
Creatine provides phosphocreatine energy buffering for motor neurons and muscles, both under bioenergetic stress in ALS.
Mechanism of Action
Creatine kinase generates phosphocreatine, buffering ATP levels during high energy demand. In ALS, motor neurons and denervated muscle fibers face energy crisis — creatine supplementation stabilizes cellular energy reserves and reduces mitochondrial-driven apoptosis.
General mechanism: Phosphocreatine energy buffer. ATP stabilization, mitochondrial protection, anti-apoptotic, muscle preservation.
Current Evidence
Phase II trials showed slowed pulmonary decline in some analyses. Phase III (NEALS consortium) did not meet primary endpoint. May benefit a subgroup of patients with preserved respiratory function.
Clinical Status: Phase III completed (negative primary endpoint). Available as supplement.
Safety Profile
Extremely safe. Decades of safety data. GI effects at high loading doses. Water retention. Safe long-term at 3-5g/day.
Key Research Questions
- Do specific ALS subtypes benefit from creatine supplementation?
- Can high-dose creatine preserve respiratory function in early ALS?