Evidence supporting the use of: SOD (Superoxide Dismutase, antioxidant activity)
For the health condition: Lou Gehrig's Disease

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Synopsis

Source of validity: Scientific
Rating (out of 5): 2

Superoxide dismutase (SOD) is an enzyme that plays a crucial role in protecting cells from oxidative damage by catalyzing the conversion of superoxide radicals into oxygen and hydrogen peroxide. Lou Gehrig’s Disease, or amyotrophic lateral sclerosis (ALS), is characterized in part by increased oxidative stress and damage to motor neurons. Notably, mutations in the gene encoding Cu/Zn SOD (SOD1) are responsible for a subset of familial ALS cases, linking the enzyme directly to disease mechanisms. This has led to scientific interest in SOD as a potential therapeutic agent for ALS. However, clinical trials evaluating SOD supplementation (usually bovine-derived SOD or synthetic mimetics) have produced disappointing results. For example, a randomized controlled trial (Appel et al., 1995, NEJM) found that intravenous bovine SOD did not slow ALS progression compared to placebo. Additionally, the bioavailability of orally administered SOD is extremely low, as the enzyme is degraded in the gastrointestinal tract. Despite its biological plausibility and direct genetic connection to ALS pathology, no robust evidence supports SOD supplementation as a beneficial therapy in ALS patients. The overall quality and quantity of evidence is low, and mainstream guidelines do not recommend SOD for ALS treatment. Research continues into SOD1-targeted therapies (such as antisense oligonucleotides), but not SOD enzyme supplementation itself. Thus, the evidence rating is 2/5, indicating initial scientific rationale but insufficient clinical benefit demonstrated.

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Other ingredients used for Lou Gehrig's Disease

omega-3 fatty acids
vitamin D

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